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Periodontal Disease and Overall Health: A Clinician's Guide

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276 <strong>Periodontal</strong> <strong>Disease</strong> <strong>and</strong> <strong>Overall</strong> <strong>Health</strong>: A <strong>Clinician's</strong> <strong>Guide</strong>Table 1. Classification of Chronic Kidney <strong>Disease</strong>GFRAction Required<strong>Disease</strong> Stage mL/min/1.73 m 2 (Additional to Previous Stage)Patient with risk factors for CKD ≥ 90 Reduce risk factors1. Kidney damage with normal or increased GFR ≥ 90 Diagnose <strong>and</strong> treatcomorbidities <strong>and</strong>CVD risk reduction2. Kidney damage with slight GFR decrease 60–89 Estimate progression3. Kidney damage with moderate GFR decrease 30–59 Treat complications4. Kidney damage with severe GFR decrease ≥ 15–29 Consider kidney replacement5. Kidney failure < 15 or Replace kidneydialysisCKD is defined as either kidney damage (pathological abnormalities in blood, urine, or imaging) or a GFR less than60 for three months or longer. (Table modified from KDOQI 2002. 11 )uremic syndrome. The uremic syndrome hasbeen associated with an increase in fatigue,anorexia, <strong>and</strong> mental status changes, <strong>and</strong> hasbeen shown to cause leukocyte dysfunction,insulin resistance, <strong>and</strong> decreased plateletfunction.Decreased kidney perfusion causes therelease of renin by granular cells in the juxta -glomerular apparatus. This release contrib -utes to the renin-angiotensin-system, leadingto multiple local <strong>and</strong> systemic effects, includingvasoconstriction, sodium reabsorption,<strong>and</strong> fluid retention. There are multipleantihypertensive agents targeting this system,including angiotensin converting enzyme(ACE) inhibitors, angiotensin II receptorblockers (ARBs), <strong>and</strong> a new class ofdirect renin inhibitors (DRIs).Patients with CKD <strong>and</strong> ESRD are at riskfor developing bone disease secondary tothe electrolyte <strong>and</strong> endocrine derangementsthat occur with decreased kidney function.As kidney disease progresses, phosphateexcretion is impaired. Additionally, there isdecreased production of active vitamin D.Vitamin D is either synthesized in the skin afterexposure to ultraviolet light or absorbedfrom dietary sources. However, vitamin Dfrom ultra violet light or dietary sources is notactive. It must undergo two hydroxylation reactionsto be activated in the body. The firsthydroxylation reaction occurs in the liver<strong>and</strong> the final hydroxylation reaction occursin the kidney. Decreased active vitamin Dlevels in combination with decreased phosphorousexcretion leads to hypocalcemia,hyperphosphatemia, <strong>and</strong> secondary hyperparathyroidism.Long-st<strong>and</strong>ing derangementsin calcium <strong>and</strong> phosphorus homeo stasiseventually lead to renal osteodystrophy,which is associated with impaired bone mineralization,increased risk of fractures, <strong>and</strong>calcification.Overview of CKDCKD is a broad term used to encompasspatients with evidence of permanentkidney damage <strong>and</strong>/or progressive decreasein kidney function as defined by glomerularfiltration rate (GFR). 11 It is estimated that 31million Americans suffer from CKD <strong>and</strong>millions of others are at risk (from National<strong>Health</strong> <strong>and</strong> Nutrition Examination Surveydata 1999-2006). The most common causesof CKD include diabetes, hypertension, <strong>and</strong>glomerulonephritis.The National Kidney Foundation haspublished staging guidelines for adult patientswith CKD. These guidelines are basedon estimated GFR, which is calculated usingthe widely accepted Modification of Dietin Renal <strong>Disease</strong> (MDRD) equation. The

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