IgA nephropathy natural history, complications and prognosis: Difference between revisions
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| bgcolor="#d9ff54"|'''Change in Serum Marker''' || bgcolor="#d9ff54"|'''Biological Marker''' | | bgcolor="#d9ff54"|'''Change in Serum Marker''' || bgcolor="#d9ff54"|'''Biological Marker''' | ||
|- | |- | ||
| bgcolor="#ececec"|'''Increase''' || *Urinary ratio of Epidermal growth factor to monocyte chemotactic peptide-1<ref name="pmid17943082">{{cite journal| author=Torres DD, Rossini M, Manno C, Mattace-Raso F, D'Altri C, Ranieri E et al.| title=The ratio of epidermal growth factor to monocyte chemotactic peptide-1 in the urine predicts renal prognosis in IgA nephropathy. | journal=Kidney Int | year= 2008 | volume= 73 | issue= 3 | pages= 327-33 | pmid=17943082 | doi=10.1038/sj.ki.5002621 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17943082 }} </ref> | | bgcolor="#ececec"|'''Increase''' || | ||
*Urinary ratio of Epidermal growth factor to monocyte chemotactic peptide-1<ref name="pmid17943082">{{cite journal| author=Torres DD, Rossini M, Manno C, Mattace-Raso F, D'Altri C, Ranieri E et al.| title=The ratio of epidermal growth factor to monocyte chemotactic peptide-1 in the urine predicts renal prognosis in IgA nephropathy. | journal=Kidney Int | year= 2008 | volume= 73 | issue= 3 | pages= 327-33 | pmid=17943082 | doi=10.1038/sj.ki.5002621 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17943082 }} </ref> | |||
*Fibroblast growth factor 23 (FGF23)<ref name="pmid22383747">{{cite journal| author=Lundberg S, Qureshi AR, Olivecrona S, Gunnarsson I, Jacobson SH, Larsson TE| title=FGF23, albuminuria, and disease progression in patients with chronic IgA nephropathy. | journal=Clin J Am Soc Nephrol | year= 2012 | volume= 7 | issue= 5 | pages= 727-34 | pmid=22383747 | doi=10.2215/CJN.10331011 | pmc=PMC3338280 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22383747 }} </ref> | *Fibroblast growth factor 23 (FGF23)<ref name="pmid22383747">{{cite journal| author=Lundberg S, Qureshi AR, Olivecrona S, Gunnarsson I, Jacobson SH, Larsson TE| title=FGF23, albuminuria, and disease progression in patients with chronic IgA nephropathy. | journal=Clin J Am Soc Nephrol | year= 2012 | volume= 7 | issue= 5 | pages= 727-34 | pmid=22383747 | doi=10.2215/CJN.10331011 | pmc=PMC3338280 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22383747 }} </ref> | ||
Line 118: | Line 119: | ||
*Uric acid<ref name="pmid22116196">{{cite journal| author=Shi Y, Chen W, Jalal D, Li Z, Chen W, Mao H et al.| title=Clinical outcome of hyperuricemia in IgA nephropathy: a retrospective cohort study and randomized controlled trial. | journal=Kidney Blood Press Res | year= 2012 | volume= 35 | issue= 3 | pages= 153-60 | pmid=22116196 | doi=10.1159/000331453 | pmc=PMC3242707 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22116196 }} </ref><ref name="pmid23391320">{{cite journal| author=Cheng GY, Liu DW, Zhang N, Tang L, Zhao ZZ, Liu ZS| title=Clinical and prognostic implications of serum uric acid levels on IgA nephropathy: a cohort study of 348 cases with a mean 5-year follow-up. | journal=Clin Nephrol | year= 2013 | volume= 80 | issue= 1 | pages= 40-6 | pmid=23391320 | doi=10.5414/CN107813 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23391320 }} </ref> | *Uric acid<ref name="pmid22116196">{{cite journal| author=Shi Y, Chen W, Jalal D, Li Z, Chen W, Mao H et al.| title=Clinical outcome of hyperuricemia in IgA nephropathy: a retrospective cohort study and randomized controlled trial. | journal=Kidney Blood Press Res | year= 2012 | volume= 35 | issue= 3 | pages= 153-60 | pmid=22116196 | doi=10.1159/000331453 | pmc=PMC3242707 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22116196 }} </ref><ref name="pmid23391320">{{cite journal| author=Cheng GY, Liu DW, Zhang N, Tang L, Zhao ZZ, Liu ZS| title=Clinical and prognostic implications of serum uric acid levels on IgA nephropathy: a cohort study of 348 cases with a mean 5-year follow-up. | journal=Clin Nephrol | year= 2013 | volume= 80 | issue= 1 | pages= 40-6 | pmid=23391320 | doi=10.5414/CN107813 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23391320 }} </ref> | ||
|- | |- | ||
| bgcolor="#ececec"|'''Decreased''' || *Soluble CD89 (sCD89)<ref name="pmid20811333">{{cite journal| author=Vuong MT, Hahn-Zoric M, Lundberg S, Gunnarsson I, van Kooten C, Wramner L et al.| title=Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy. | journal=Kidney Int | year= 2010 | volume= 78 | issue= 12 | pages= 1281-7 | pmid=20811333 | doi=10.1038/ki.2010.314 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20811333 }} </ref> | | bgcolor="#ececec"|'''Decreased''' || *Soluble CD89 (sCD89)<ref name="pmid20811333">{{cite journal| author=Vuong MT, Hahn-Zoric M, Lundberg S, Gunnarsson I, van Kooten C, Wramner L et al.| title=Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy. | journal=Kidney Int | year= 2010 | volume= 78 | issue= 12 | pages= 1281-7 | pmid=20811333 | doi=10.1038/ki.2010.314 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20811333 }} </ref>|} | ||
==References== | ==References== |
Revision as of 16:57, 21 October 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Natural History
The clinical course of IgA nephropathy varies widely between patients. Although it is generally regarded as a benign disease, emerging data has shown that progression to ESRD and death are more common than originally believed.[1] Some patients rapidly progress into ESRD; but the majority experience a stable kidney function following diagnosis.[1] Commonly, the progression of IgA nephropathy is slower than other notorious glomerular disease. Approximately 20-30% of patients with IgA nephropathy progress to ESRD after 10 years[1] and up to 30-50% of patients develop ESRD over 20 years.[2][3]
Complications
Complications of IgA nephropathy are generally those of renal injury.
- Hypertension
- Nephritic syndrome
- Nephrotic syndrome
- Acute kidney injury
- Chronic kidney disease
- End-stage renal disease
- Hypercholesterolemia
Prognosis
IgA nephropathy follows an unpredictable clinical course with debatable prognostic factors. Although considered a benign disease in comparison to other forms of glomerulonephritis, new data show that up to 20-30% of patients with IgA nephropathy progress to ESRD after 10 years.[1] It is important, however, to note that experts concede that the true prognosis of IgA nephropathy is poorly established because the diagnosis by biopsy is often made late during stage 3-4 chronic kidney disease.[3] The approximately 10-year renal survival following diagnosis ranges between 67-94%, based on the findings of 5 major trials from Germany, France, UK, Japan, and Australia and 1 meta-analysis from USA.[4][5][6][7][8]
Several studies have analyzed factors associated with prognosis of IgA nephropathy. In 2011, Berthoux and colleagues established 3 main factors that have been attributed to be the core predictors of outcome when studying 332 patients with IgA nephropathy over 13 years[9]:
1- Proteinuria > 1g/24 hrs
2- Severe pathologic lesions with a global optical score ≥ 8
3- Hypertension > 140/90 mmHg
Proteinuria is the most important prognostic factor with a “dose-dependent” effect[10]
In 2011, Berthoux et al. calculated absolute renal risk (ARR) of dialysis or death.[9] The absence of all 3 risk factors was associated with a 96% prediction of survival without hemodialysis.[9] As ARR increased, survival prediction decreased, where the presence of all 3 risk factors was associated with only 36% prediction of survival without the need for dialysis.[9]
In one major meta-analysis that involved a database of 148 patients with IgA nephropathy between 1973 and 1995, Radford and colleagues[3] suggested a “glomerular score” based on previous findings from the literature that consists of the summation of 6 components:
- Mesangial hypercellularity
- Mesangial matrix increase
- Glomerular sclerosis
- Capillary narrowing or disruption
- Cellular crescents
- Fibrous adhesions
Observational, cross-sectional, and cohort studies to date have shown the following data to be significantly associated with progression of IgA nephropathy into ESRD and worse outcome. However, the significance of the following is variable and has not been consistent in the literature.
Genetic:
- D or DD allele of insertion/deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE) gene[11]
Clinical:
- Smoking
- Metabolic Syndrome
Biochemical
- Elevated serum creatinine levels at diagnosis[3]
- Persistence of microscopic hematuria[3]
- Hypertriglyceridemia[12]
- Hyperuricemia[12]
- Anemia[13]
- Hypoalbuminemia[13]
Histopathological
- Tubular atrophy
Age remains a controversial predictor of outcome for patients with IgA nephropathy. While some studies showed that younger age is associated with worse outcomes[3], these findings were not consistent in the literature and at times, completely opposing.[16][4]