Intervention
| Goal/Comment
|
| 1. Control BP (Level 1) | The goal is a sitting systolic BP in the 120s or less, if tolerated. The greater the proteinuria, the greater the benefit of the low goal. Text has recommended antihypertensive regimens. |
| 2. ACEI therapy (Level 1) | Use ACEI even if normotensive. ACEI is first choice because of proven cardio protection. Use maximum recommended doses if tolerated. Goal is proteinuria <0.5 g/d. |
| 3. ARB therapy (Level 1) | Proven antiproteinuric and renoprotective therapy. Studies are underway to assess cardiovascular protection compared with ACEI. ARB is first choice if ACEI-intolerant. Use maximum recommended doses, if tolerated. Goal is proteinuria <0.5 g/d. |
| 4. Combination ACEI and ARB therapies (Level 1) | Adding ARB to maximum ACEI appears to reduce proteinuria further. However, BP may not be reduced further. |
| 5. Avoid DHCCB unless needed for BP control (Level 1) | DHCCBs are excellent antihypertensive agents but they are not antiproteinuric and may promote kidney disease progression. ARB therapy may mitigate these effects. |
| 6. beta-blocker therapy (Level 1) | beta-blocker therapy is antiproteinuric compared to DHCCB-therapy. |
| 7. Control protein intake (Level 1) | Goal is 0.7 to 0.8 g/kg/d. Effect on proteinuria is nearly the same as that of the low BP goal. Soy proteins may offer advantages over other protein sources. |
| 8. Restrict NaCl intake (Level 2) (Level 1 for BP control) | Goal is 80 to 120 mmol/d ( 2.0 to 3.0 g Na) to optimize the antiproteinuric effects of ACEI, ARB, or NOH-CCB therapy. Lower salt intake controls BP, which may further reduce proteinuria. |
| 9. Control fluid intake (Level 2) | Goal is urine volume <2.0 L/d unless higher fluid intake is needed for specific reasons. In the MDRD Study A, each 1% greater urine volume was associated with a 1% increase in urine protein/creatinine ratio. Also, urine volumes >2.0 L/d were associated with faster GFR decline. |
| 10. NDH-CCB therapy (Level 2) | This CCB class is antiproteinuric. It might also be renal protective based on observational studies. |
| 11. Control blood lipids (Level 2) (Level 1 for cardiovascular benefit) | There is good evidence that statins are antiproteinuric and renoprotective. |
| 12. Aldosterone antagonist therapy (Level 2) | Spironolactone is antiproteinuric in humans and in animal models independent of BP control. |
| 13. Smoking cessation (Level 2) | Cigarette smoking in humans increases proteinuria/albuminuria and is associated with faster kidney disease progression. Smoke condensate worsens proteinuria and glomerulosclerosis in experimental kidney disease in rats. |
| 14. Avoid estrogen/progestin replacement therapy in postmenopausal women with kidney disease (Level 2) | Estrogens may have renoprotective effects that explain slower progression of kidney disease in premenopausal women compared with men of the same age. However, estrogens induce microalbuminuria and have other adverse effects in postmenopausal women. |
| 15. Supine/recumbent posture when feasible. Avoid severe exertion (Level 2) | Nephrotic-range proteinuria decreases by as much as 50% during recumbency. Severe exercise may increase proteinuria substantially. |
| 16. Reduce obesity (Level 2) | Obesity apparently causes glomerulomegaly and proteinuria. Reducing obesity reduces proteinuria. |
| 17. Decrease elevated homocysteine (Level 3) | Hyperhomocystinuria is associated with microalbuminuria and increased cardiovascular risks. Folic acid, B6, and B12 may lower homocysteine levels. |
| 18. Antioxidant therapies (Level 3) | Antioxidant therapies of several types reduce proteinuria in both experimental models and in patients with diabetic nephropathy. |
| 19. Sodium bicarbonate therapy to correct metabolic acidosis (Level 3) | NaHCO3 therapy is not antiproteinuric; however, it blocks complement activation in the tubular compartment and, therefore, may block tubular injury caused by proteinuria. Correction of metabolic acidosis also decreases protein catabolism, which may provide general benefit. |
| 20. NSAID therapy in severe untreatable nephrotic syndrome (Level 3) | NSAIDs (both COX 2 and nonspecific COX inhibitors) are antiproteinuric but are also nephrotoxic. Thus, NSAID use should be reserved for severe untreatable nephrotic syndrome to reduce proteinuria and achieve symptomatic relief. |
| 21. Other therapies based on animal studies (Level 3) | Avoid excessive caffeine, iron overload. Allopurinol, pentoxifylline, mycophenolate therapy. See text. |