Monday, June 3, 2013

A Brief Synopsis of AFP's "Update on the Management of Chronic Kidney Disease"

A brief synopsis of:
Update on the Management of Chronic Kidney Disease
JOSETTE A. RIVERA, MD, University of California, San Francisco, California, ANN M. O’HARE, MD, University of Washington, Seattle, Washington, G. MICHAEL HARPER, MD, University of California, San Francisco, California 
Am Fam Physician. 2012 Oct 15;86(8):749-754
http://www.aafp.org/afp/2012/1015/p749.pdf

     Chronic kidney disease (CKD) is defined by a GFR less than 60ml/min/1.73 m2, or three or more months of kidney damage regardless of GFR. Staging is based mostly on GFR. Patients with CKD more often die from cardiovascular disease (CVD) than require dialysis. For this reason, cardiovascular disease management is an important aspect in treating patients with CKD.
     Diabetes is the leading cause of CKD, as well as a risk factor for CVD. Current recommendations suggest an A1C level of less than 7% in patients without proteinuria. This may be too aggressive because of a higher rate of complications such as hypoglycemia, without any proven reduction in mortality, need for dialysis or cardiovascular events.
     Proteinuria is a risk factor for all-cause and cardiovascular mortality. Patients with diabetic kidney disease, or nondiabetic kidney disease with a protein-to-creatinine ratio greater than 200 mg/g, should be started on an ACEI or ARB. Patients without proteinuria may not benefit from the medication.  Combinations of ACEI and ARBs have not shown any outcome benefit, but have shown increased adverse effects, including decreasing renal function.
     The JNC 7 has recommended a BP of less than 130/80 in patients with CKD. Studies show no benefit compared to a BP of 140-160/90-100. It may have benefit in patients with proteinuria over 300 mg/day.
     Raising hemoglobin can adversely affect patients with CKD. Target levels above 13.3 g/dL can cause a higher risk of all-cause mortality, stroke, and cardiovascular death. Target levels should stay at 11-12 g/dL. Treatment can be administered at levels less than 10 g/dL, or during an acute drop in hemoglobin triggering the need for a transfusion.
     Imaging contrast can affect patients with CKD. Patients with a GFR less than 60 mL/min are at an increased risk of contrast induced nephropathy. It is seen as a rise in creatinine greater than 25% above normal or an increase of 0.5 mg/dL. This will occur within a few days after the contrast is used.  Patients can minimize the risk of nephropathy with adequate hydration and avoiding NSAIDs. IV hydration with sodium bicarb or NS can reduce the risk as well. N-ac has had inconsistent results as a preventative tool for contrast induced nephropathy. It is a relatively cheap and safe medication with little risk to use as an adjunct. Gadolinium-based contrast in MRI has been associated with kidney injury and fibrosis. It should not be used in patients with a GFR less than 30 ml/min/1.73m2.
   

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