Natural course of chronic kidney disease 1 2 Factors affecting renal disease progression 3 5 1 Fig. 1 EPO P reduction RAS Non-DHP CCP TGFβ TIMP ET1 PAI ⊥  Hypertension 3 5 6 7 8 9 10 11 12 13 14 15 15 16 17 18 19 Proteinuria 20 22 23 25 26 9 27 28 29 30 25 31 33 2 25 34 35 36 2 Dyslipidemia 37 38 39 40 41 37 37 42 Anemia 43 44 45 Oxidative stress 46 Nutrition 47 Disorders of calcium-phosphate metabolism 48 Treatment strategies and their impact on renal disease progression 25 49 32 25 49 2 35 36 32 35 50 51 Blockade of the renin-angiotensin system 15 8 52 35 31 35 53 61 51 62 63 64 65 66 35 36 67 69 32 70 71 72 73 74 2 17 28 75 76 77 78 79 Calcium-channel blockers 33 70 33 80 81 Beta-blockers 54 32 82 83 Combination therapy 13 64 84 86 64 87 88 Restoration of blood pressure day–night rhythm 89 90 91 Treatment of dyslipidemia 92 94 95 96 97 98 99 100 Erythropoietin treatment 101 102 103 104 Nutrition and vitamin D supplementation 105 106 9 107 108 109 3 110 111 109 Conclusion In conclusion, hypertension and proteinuria are key players in renal disease progression. Therapeutic strategies to prevent progression should comprise blood pressure control and lowering of proteinuria. RAS antagonists preserve kidney function, not only by lowering blood pressure but also through antiproteinuric and antifibrotic properties. Other factors contributing to renal disease progression in a multifactorial manner include anemia, dyslipidemia, and disorders of mineral metabolism, and measures to preserve renal function should therefore also comprise the maintenance of hemoglobin and serum lipid and calcium-phosphorus ion product levels in the normal range. Questions (Answers appear following the reference list.) Declines linearly Nonlinearly and often characterized by a sharp decline in renal function during puberty Inevitably Strongly, depending upon the underlying renal disease Results in ESRD in less than 50% of patients at age 20 years Age at onset of chronic renal failure, gender, and underlying renal disease Residual renal function and blood pressure Blood pressure and proteinuria Rapid somatic growth during puberty, and age Antihypertensive efficacy Antiproteinuric efficacy Side effects and safety profile Effect on CKD progression Strictly dose dependent Basically mediated by reduction of systemic hypertension Mediated by bradykinin release Also mediated by antifibrotic and vasodilatory effects Due to restoration of the often disturbed day–night blood pressure pattern (dipping) in CKD patients Are approved for the indication proteinuria and hypertension Do not exert additional antiproteinuric effect when combined with ACE inhibitors Should be given at the highest approved dose for maximal antiproteinuric effect Should not be combined with ACE inhibitors Have the same side effect profile as ACE inhibitors Is independent of serum cholesterol level Can be reversed by dietary protein restriction Can be reversed by the use of statins in younger children May be accelerated by prescription of erythropoietin May be retarded by the lipid-independent pleiotropic anti-inflammatory effects of statins