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S28 Introduction S30 Summary of recommendation statements and practice points S88 Chapter 1: General principles for the management of glomerular disease S115 Chapter 2: Immunoglobulin A nephropathy (IgAN)/immunoglobulin A vasculitis (IgAV) S128 Chapter 3: Membranous nephropathy S140 Chapter 4: Nephrotic syndrome in children S153 Chapter 5: Minimal change disease (MCD) in adults S161 Chapter 6: Focal segmental glomerulosclerosis (FSGS) in adults S172 Chapter 7: Infection-related glomerulonephritis S187 Chapter 8: Immunoglobulin-and complement-mediated glomerular diseases with a membranoproliferative glomerulonephritis (MPGN) pattern of injury S193 Chapter 9: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis S207 Chapter 10: Lupus nephritis S231 Chapter 11: Anti-glomerular basement membrane (Anti-GBM) antibody glomerulonephritis S235 Methods for guideline development S243 Biographic and disclosure information S254 Acknowledgments S256 ReferencesThis guideline is published as a supplement supported by KDIGO. The development and publication of this guideline are strictly funded by KDIGO, and neither KDIGO nor its guideline Work Group members sought or received monies or fees from corporate or commercial entities in connection with this work. The opinions or views expressed in this professional education supplement are those of the authors and do not necessarily reflect the opinions or recommendations of the International Society of Nephrology or Elsevier. Dosages, indications, and methods of use for products that are referred to in the supplement by the authors may reflect their clinical experience or may be derived from the professional literature or other clinical sources. Because of the differences between in vitro and in vivo systems and between laboratory animal models and clinical data in humans, in vitro and animal data may not necessarily correlate with clinical results.

Our study supports the concept that proteinuria is an independent risk factor for the progression of renal disease. For patients with proteinuria of more than 1 g/d, we suggest a target blood pressure of less than 92 mm Hg (125/75 mm Hg). For patients with proteinuria of 0.25 to 1.0 g/d, a target mean arterial pressure of less than 98 mm Hg (about 130/80 mm Hg) may be advisable. The extent to which lowering blood pressure reduces proteinuria may be a measure of the effectiveness of this therapy in slowing the progression of renal disease.

End stage renal disease (ESRD) has a four times higher incidence in African Americans compared to European Americans. This led to the hypothesis that susceptibility alleles for ESRD have a higher frequency in West African than European gene pool. We performed a genome-wide admixture scan in 1,372 ESRD cases and 806 controls and demonstrated a highly significant association between excess African ancestry and non-diabetic ESRD (LOD 5.70) but not diabetic ESRD (LOD 0.47) on chromosome 22q12. Each copy of the European ancestral allele conferred a relative risk of 0.50 (95% credible interval 0.39 -0.63) compared to African ancestry. Multiple common SNPs (allele frequency ranging from 0.2 to 0.6) in the gene that encodes non-muscle myosin heavy chain type II isoform A (MYH9) were associated with 2-4 times greater risk of non-diabetic ESRD and accounted for a large proportion of the excess risk of ESRD observed in African compared to European Americans.End stage renal disease (ESRD) is the near-total loss of kidney function requiring treatment of 472,000 patients with dialysis or transplantation in the US 1 . Diabetes and hypertension are the two leading reported causes of treated ESRD in the U.S. accounting for 44% and 27% of incident cases respectively 1 . African Americans have consistently had a much higher rate of ESRD than European Americans in the US. In 2005, African-Americans had a 3.7 times higher age adjusted risk of ESRD. The risk ratio by assigned primary cause of ESRD was 3.8 for hypertension, 2.6 for diabetes, 2.3 for glomerulonephritis, 2.1 for the other causes of kidney disease 1 . While lower socioeconomic status and poorer access to health care explains some of this excess risk 2-4 , African Americans appear to have greater risk than European Americans after these factors are taken into account. Family studies show clustering of ESRD independent of hypertension and diabetes 5, 6 with one large study shows stronger aggregation in African Americans 6 . Studies attempting to detect susceptibility genes for ESRD and other complex diseases are challenging due to the late age of onset, causing difficulty in collecting multiply-affected families, and because linkage analysis has suggested that there are no genes of high penetrance (>4-fold increased risk) in populations of European descent, the focus of most published studies 7, 8 . For these reasons, ESRD is an excellent phenotype for whole genome association analysis, an approach with enhanced power to detect common variants of modest penetrance, and with the further advantage that unrelated individuals can be studied.We performed a scan for ESRD genes using a particular type of whole genome association analysis, termed admixture mapping or mapping by admixture linkage disequilibrium (MALD) Linda NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript 9-11 . Admixture mapping is particularly suitable for finding genetic risk alleles that differ in frequency between populations which we hypothesized might be the case for ESRD.The...

The Modification of Diet in Renal Disease (MDRD) Study examined the effects of dietary protein restriction and strict blood pressure control on the decline in glomerular filtration rate (GFR) in 840 patients with diverse renal diseases. We describe a systematic analysis to determine baseline factors that predict the decline in GFR, or which alter the efficacy of the diet or blood pressure interventions. Univariate analysis identified 18 of 41 investigated baseline factors as significant (P < 0.05) predictors of GFR decline. In multivariate analysis, six factors--greater urine protein excretion, diagnosis of polycystic kidney disease (PKD), lower serum transferrin, higher mean arterial pressure, black race, and lower serum HDL cholesterol--independently predicted a faster decline in GFR. Together with the study interventions, these six factors accounted for 34.5% and 33.9% of the variance between patients in GFR slopes in Studies A and B, respectively, with proteinuria and PKD playing the predominant role. The mean rate of GFR decline was not significantly related to baseline GFR, suggesting an approximately linear mean GFR decline as renal disease progresses. The 41 baseline predictors were also assessed for their interactions with the diet and blood pressure interventions. A greater benefit of the low blood pressure intervention was found in patients with higher baseline urine protein. None of the 41 baseline factors were shown to predict a greater or lesser effect of dietary protein restriction.