progression to ESRD. Comprehensive systems targeting early recognition, prevention and management, and treatment by primary care physicians and physician extenders are required at this critical stage in collaboration with nephrologists. 9 Aside from uncontrolled HTN, one of the strongest prognosticators for declining kidney function is proteinuria. A “spot” urine protein-to-creatinine ratio (UPC) or urine albumin-to-creatinine ratio (UACR) quantifies proteinuria. Generally, UPCs 1 predict more rapid functional decline and more intensive evaluation, ie, kidney biopsy. Modifiable risk factors for CKD progression are HTN, diabetes, morbid obesity, metabolic syndrome, hypercholesterolemia, heavy consumption of non-narcotic analgesic preparations, anemia, and cigarette smoking. Perhaps the best prognosticator for CKD progression is the rate of decline of GFR. Rates of decline >4 mL/min/1.73 m2 per year are associated with greater progression risk. In diabetics, annual eGFR rates of decline 10–12 mL/min/1.73 m2 may occur. In heart failure, eGFR declines 15 mL/min/1.73 m2 per year are associated with worse anemia and progression to CKD Stage 5. African American ethnicity is a major risk factor for progressive CKD from type 2 diabetic kidney disease, HTN (nephrosclerosis), and HIV. In general, Native Americans, Hispanics, and Asians have increased risk for type 2 diabetic CKD. Cigarette smoking aggravates CKD. Risk factors that promote the accelerated atherosclerosis of CKD include elevated angiotensin II levels, proteinuria, secondary hyperparathyroidism, dysregulated calcium and phosphate metabolism, ECF volume expansion, and the intrinsic chronic inflammatory state of CKD. Strategies that retard the progression of CKD includes optimizing antihypertensive therapy; stringent glycemic control; cigarette smoking cessation; avoidance of cocaine, NSAIDs, and exposure to nephrotoxic agents; and dietary protein and phosphorus restrictions. FACTOR-SPECIFIC INTERVENTIONS TO REDUCE RISK OF CKD PROGRESSION Classification Definition Risk Factor Category 1 Factor-specific intervention reduces risk Diabetes, hypertension, obesity, metabolic syndrome, hyperlipidemia Category 2 Factor-specific intervention likely reduces risk Smoking, cocaine, nephrotoxic exposure (certain drugs), kidney stones, prostatic hypertrophy (obstruction), radiocontrast media Category 3 Factor-specific modification may lower risk High protein intake, obesity, metabolic syndrome, low income and/or educational level, chemical and environmental hazards (lead) Category 4 Factor-specific modification not possible Advanced age, male gender, ethnicity (African American, Native American, Hispanic, and Asian), family history of CKD (cystic kidney disease), low birth weight, congenital or acquired solitary kidney, and prior kidney damage (trauma, infection) 10 COMMENTS • Determine whether AKI is present in all cases of CKD. • Evaluate and correct all potentially reversible causes of reduced GFR. • A partial list of common causes of AKI with acute GFR reductions follows. a) Altered intrarenal hemodynamics: common agents that decrease GFR, eg, NSAIDs (COX-1/-2 inhibitors), ACEIs, and ARBs. b) Drug-induced acute tubulointerstitial nephritis: commonly implicated agents include penicillins, cephalosporins, sulfonamides, rifampin, phenytoin, fluoroquinolones and NSAIDs (non-hemodynamically related ARF). c) ECF volume depletion, especially with NSAID, ACEI, or ARB drug co-administration d) Heart failure e) Hypotension f) Liver disease g) Nephrotoxins: aminoglycosides, pentamadine, foscarnet, amphotericin, cis-platinol, and multiple chemotherapeutic agents h) Radiocontrast medium (eg, iodine- or gadolinium-based contrast agent-containing diagnostic procedures) i) Rhabdomyolysis j) Urinary tract outlet obstruction must always be ruled out, particularly in males REFERENCES 1. AS Levey, et al. Ann Int Med 130: 461, 1999 2. NKF KDOQI clinical practice guidelines for CKD. Am J Kidney Dis 39(Suppl 1): S76, 2002 3. K Iseki, et al. Kidney Int 64: 1468, 2003 4. K Klausen, et al. Circulation 110: 32, 2004 5. J Lea, et al. Arch Int Med 165: 947, 2005 6. AS Levey, et al. Ann Int Med 145: 247, 2006 7. AS Go, et al. N Engl J Med 351: 1296, 2004 8. E Selvin, et al. Am J Kidney Dis 50: 918, 2007 9. J Yee. Geriatrics 63(3):30, 2008 10. SI Hallan, et al. J Am Soc Nephrol 20: 1069, 2009 11. BR Hemmelgarn, et al. JAMA 303: 423, 2010 12. M Tonelli, et al. Annals Int Med 154(1): 12, 2011 13. S Herget-Rosenthal et al. Int J Clin Pract 64(13):1784, 2010 11 CONSULTATION by Jerry Yee Introduction In a survey, family medicine physicians (N=89), general internists (N=89), and nephrologists (N=129) evaluated a case of progressive CKD. Family medicine and internal medicine doctors recognized and recommended subspecialist care for progressive CKD less frequently than nephrologists. Their opinions also differed from nephrologists regarding evaluations by and expectations of nephrologists. The survey recommended the following: a) greater dissemination of existing clinical practice guidelines b) targeted CKD-specific education c) consensus-building and guideline development by family medicine physicians, internists, and nephrologists. Data from dedicated CKD clinics corroborate these findings. Currently, there is a concerted effort from many nephrology societies, including AMA, AHRQ,