Membranoproliferative glomerulonephritis laboratory findings: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Membranoproliferative glomerulonephritis}} | {{Membranoproliferative glomerulonephritis}} | ||
{{CMG}} | {{CMG}} {{JSS}} | ||
==Overview== | ==Overview== | ||
MPGN laboratory findings include urinalysis, renal function tests, complete blood counts, complement profile and other diagnostic tests for evaluating the cause of MPGN. | MPGN laboratory findings include [[urinalysis]], [[renal function tests]], [[Complete blood count|complete blood counts]][[Complement|, complement profile]] and other diagnostic tests for evaluating the cause of MPGN. | ||
==Laboratory Findings== | ==Laboratory Findings== | ||
=== Urinalysis === | === Urinalysis === | ||
:* Glomerular hematuria; characterized by dysmorphic red blood cells (RBCs) and RBC casts<ref name="pmid22435371">{{cite journal| author=Sethi S, Fervenza FC| title=Membranoproliferative glomerulonephritis--a new look at an old entity. | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 12 | pages= 1119-31 | pmid=22435371 | doi=10.1056/NEJMra1108178 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22435371 }} </ref> | :* Glomerular [[hematuria]]; characterized by dysmorphic red blood cells (RBCs) and [[Urinary casts|RBC casts]]<ref name="pmid22435371">{{cite journal| author=Sethi S, Fervenza FC| title=Membranoproliferative glomerulonephritis--a new look at an old entity. | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 12 | pages= 1119-31 | pmid=22435371 | doi=10.1056/NEJMra1108178 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22435371 }} </ref> | ||
:* Proteinuria is almost always present. | :* [[Proteinuria]] is almost always present. | ||
:* Urine protein creatinine ratio is a good estimate of 24-hour urinary protein excretion. | :* Urine protein creatinine ratio is a good estimate of 24-hour urinary protein excretion. | ||
:* Nephrotic proteinuria is present in approximately 50% of patients. | :* Nephrotic proteinuria is present in approximately 50% of patients. | ||
=== Serum chemistries === | === Serum chemistries === | ||
:* Elevated serum creatinine and blood urine nitrogen and a decreased estimated glomerular filtration rate (GFR) are evident in 20-50% of patients at presentation. Patients with a nephritic presentation typically have a decreased GFR<ref name="pmid7723253">{{cite journal| author=Rennke HG| title=Secondary membranoproliferative glomerulonephritis. | journal=Kidney Int | year= 1995 | volume= 47 | issue= 2 | pages= 643-56 | pmid=7723253 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7723253 }} </ref>. | :* Elevated serum [[creatinine]] and blood urine nitrogen and a decreased estimated [[glomerular filtration rate]] (GFR) are evident in 20-50% of patients at presentation. Patients with a [[Nephritic syndrome|nephritic]] presentation typically have a decreased GFR<ref name="pmid7723253">{{cite journal| author=Rennke HG| title=Secondary membranoproliferative glomerulonephritis. | journal=Kidney Int | year= 1995 | volume= 47 | issue= 2 | pages= 643-56 | pmid=7723253 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7723253 }} </ref>. | ||
:* Hyperlipidemia and low albumin may be seen with nephrotic syndrome. | :* [[Hyperlipidemia]] and low [[albumin]] may be seen with [[nephrotic syndrome]]. | ||
=== CBC with differential: === | === CBC with differential: === | ||
* Most often, patients have a normocytic normochromic anemia. | * Most often, patients have a [[Anemia|normocytic normochromic anemia]]. | ||
=== Complement profile - === | === Complement profile - === | ||
* MPGN type I<ref name="pmid18408474">{{cite journal| author=Alpers CE, Smith KD| title=Cryoglobulinemia and renal disease. | journal=Curr Opin Nephrol Hypertens | year= 2008 | volume= 17 | issue= 3 | pages= 243-9 | pmid=18408474 | doi=10.1097/MNH.0b013e3282f8afe2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18408474 }} </ref> | * MPGN type I<ref name="pmid18408474">{{cite journal| author=Alpers CE, Smith KD| title=Cryoglobulinemia and renal disease. | journal=Curr Opin Nephrol Hypertens | year= 2008 | volume= 17 | issue= 3 | pages= 243-9 | pmid=18408474 | doi=10.1097/MNH.0b013e3282f8afe2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18408474 }} </ref> | ||
:* C3 levels are low in about half of the patients. | :* [[C3-convertase|C3]] levels are low in about half of the patients. | ||
:* Evidence of activation of the classic pathway of complement (ie, low C4, C2, C1q, B, C3) | :* Evidence of activation of the classic pathway of [[complement]] (ie, low C4, C2, C1q, B, C3) | ||
:* Terminal complement components C3, C5, C8, and C9 may be low or within the reference range. | :* Terminal complement components C3, C5, C8, and C9 may be low or within the reference range. | ||
:* NFc (C4NeF) or NFt may be present. | :* NFc (C4NeF) or NFt may be present. | ||
* MPGN type II | * MPGN type II | ||
:* C3 levels are low in 70-80% of patients. | :* C3 levels are low in 70-80% of patients. | ||
:* Early and terminal | :* Early and terminal [[Complement|complemen]]<nowiki/>t components are within the reference range. | ||
:* NFa (C3NeF) is present in more than 70% of patients. | :* NFa (C3NeF) is present in more than 70% of patients. | ||
* MPGN type III | * MPGN type III | ||
| Line 36: | Line 36: | ||
:* NFa is absent and NFt is present in 60-80% of patients. | :* NFa is absent and NFt is present in 60-80% of patients. | ||
:* Antistreptolysin-O (ASO) titers may be elevated in as many as 50% of patients at presentation. | :* Antistreptolysin-O (ASO) titers may be elevated in as many as 50% of patients at presentation. | ||
* To rule out secondary causes, obtain antinuclear antibodies, hepatitis screens, | * To rule out secondary causes, obtain [[antinuclear antibodies]], [[hepatitis]] screens, [[Cryoglobulinemia|cryoglobulin]]<nowiki/>s, urine, and serum protein electrophoresis. | ||
==References== | ==References== | ||
Revision as of 17:26, 30 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Jogeet Singh Sekhon, M.D. [2]
Overview
MPGN laboratory findings include urinalysis, renal function tests, complete blood counts, complement profile and other diagnostic tests for evaluating the cause of MPGN.
Laboratory Findings
Urinalysis
- Glomerular hematuria; characterized by dysmorphic red blood cells (RBCs) and RBC casts[1]
- Proteinuria is almost always present.
- Urine protein creatinine ratio is a good estimate of 24-hour urinary protein excretion.
- Nephrotic proteinuria is present in approximately 50% of patients.
Serum chemistries
- Elevated serum creatinine and blood urine nitrogen and a decreased estimated glomerular filtration rate (GFR) are evident in 20-50% of patients at presentation. Patients with a nephritic presentation typically have a decreased GFR[2].
- Hyperlipidemia and low albumin may be seen with nephrotic syndrome.
CBC with differential:
- Most often, patients have a normocytic normochromic anemia.
Complement profile -
- MPGN type I[3]
- C3 levels are low in about half of the patients.
- Evidence of activation of the classic pathway of complement (ie, low C4, C2, C1q, B, C3)
- Terminal complement components C3, C5, C8, and C9 may be low or within the reference range.
- NFc (C4NeF) or NFt may be present.
- MPGN type II
- C3 levels are low in 70-80% of patients.
- Early and terminal complement components are within the reference range.
- NFa (C3NeF) is present in more than 70% of patients.
- MPGN type III
- C3 levels are decreased in 50% of patients.
- C1q and C4 levels are within the reference range.
- Terminal complement components are low, especially if C3 is markedly depressed.
- NFa is absent and NFt is present in 60-80% of patients.
- Antistreptolysin-O (ASO) titers may be elevated in as many as 50% of patients at presentation.
- To rule out secondary causes, obtain antinuclear antibodies, hepatitis screens, cryoglobulins, urine, and serum protein electrophoresis.
References
- ↑ Sethi S, Fervenza FC (2012). "Membranoproliferative glomerulonephritis--a new look at an old entity". N Engl J Med. 366 (12): 1119–31. doi:10.1056/NEJMra1108178. PMID 22435371.
- ↑ Rennke HG (1995). "Secondary membranoproliferative glomerulonephritis". Kidney Int. 47 (2): 643–56. PMID 7723253.
- ↑ Alpers CE, Smith KD (2008). "Cryoglobulinemia and renal disease". Curr Opin Nephrol Hypertens. 17 (3): 243–9. doi:10.1097/MNH.0b013e3282f8afe2. PMID 18408474.