Rapidly progressive glomerulonephritis laboratory findings: Difference between revisions
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{{Rapidly progressive glomerulonephritis}} | {{Rapidly progressive glomerulonephritis}} | ||
{{CMG}}; {{AE}} {{MAD}} {{N.F}} | {{CMG}}; {{AE}} {{MAD}} {{N.F}} | ||
==Overview== | ==Overview== | ||
The most important step in managing rapidly progressive glomerulonephritis is rapid diagnosis. It is essential for organ preservation. Laboratory studies include, | The most important step in managing rapidly progressive glomerulonephritis is rapid diagnosis. It is essential for organ preservation. Laboratory studies include, | ||
complete blood cell count (CBC) with differential, serum electrolytes, BUN, creatinine, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), and liver function tests: The most common abnormality is an increased serum creatinine level. However, the level can be normal at presentation. Tissue enzyme (ie, LDH, CPK) levels may be elevated if there is | [[complete blood cell count]] (CBC) with differential, [[serum electrolytes]], BUN, [[creatinine]], [[lactate dehydrogenase]] (LDH), [[creatine phosphokinase]] (CPK), and [[liver function tests]]: The most common abnormality is an increased [[serum creatinine]] level. However, the level can be normal at presentation. Tissue enzyme (ie, LDH, CPK) levels may be elevated if there is significant muscle inflammation and [[myalgias]]. [[Urinalysis]] with microscopy usually show [[proteinuria]] but is rarely greater than 2-3 g in 24 hours. [[Microscopic hematuria]] may be present and may be the only clue to renal disease at presentation. The presence of [[red cell casts]] indicates [[glomerulonephritis]] and is a very helpful clue. [[Erythrocyte sedimentation rate]] is usually elevated with active disease. [[C-reactive protein]] levels are elevated and correspond with disease activity. High [[antinuclear antibody]] (ANA) titer rises the suspicion toward [[systemic lupus erythematosus]]. More than 80% of patients with [[microscopic polyangiitis]] are ANCA-positive. The symptoms of [[cryoglobulinemia]] are very similar to those of ANCA-related disease. However, in persons with ANCA-related diseases, the [[cryoglobulin]] titer result should be negative. [[Hepatitis]] profile should be performed as hepatitis B is associated with [[polyarteritis nodosa]] and [[hepatitis C]] is associated with [[mixed cryoglobulinemia]]. Urine and serum [[protein electrophoresis]] is done in any middle-aged or elderly person presenting with rapidly progressive glomerulonephritis to exclude the presence of [[light-chain disease]] or noticeable [[multiple myeloma]] as a cause of the clinical findings. | ||
==Laboratory Findings== | ==Laboratory Findings== | ||
Revision as of 14:13, 31 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2] Nazia Fuad M.D.
Overview
The most important step in managing rapidly progressive glomerulonephritis is rapid diagnosis. It is essential for organ preservation. Laboratory studies include, complete blood cell count (CBC) with differential, serum electrolytes, BUN, creatinine, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), and liver function tests: The most common abnormality is an increased serum creatinine level. However, the level can be normal at presentation. Tissue enzyme (ie, LDH, CPK) levels may be elevated if there is significant muscle inflammation and myalgias. Urinalysis with microscopy usually show proteinuria but is rarely greater than 2-3 g in 24 hours. Microscopic hematuria may be present and may be the only clue to renal disease at presentation. The presence of red cell casts indicates glomerulonephritis and is a very helpful clue. Erythrocyte sedimentation rate is usually elevated with active disease. C-reactive protein levels are elevated and correspond with disease activity. High antinuclear antibody (ANA) titer rises the suspicion toward systemic lupus erythematosus. More than 80% of patients with microscopic polyangiitis are ANCA-positive. The symptoms of cryoglobulinemia are very similar to those of ANCA-related disease. However, in persons with ANCA-related diseases, the cryoglobulin titer result should be negative. Hepatitis profile should be performed as hepatitis B is associated with polyarteritis nodosa and hepatitis C is associated with mixed cryoglobulinemia. Urine and serum protein electrophoresis is done in any middle-aged or elderly person presenting with rapidly progressive glomerulonephritis to exclude the presence of light-chain disease or noticeable multiple myeloma as a cause of the clinical findings.
Laboratory Findings
Blood Work-Up
- Complete blood count (CBC)
- Anemia
- Eosinophilia
- Serum electrolytes
- Lactate dehydrogenase (LDH)
- Creatine phosphokinase (CPK)
- Antinuclear antibody (ANA)
- Complement C3 and C4 levels
- Serum protein electrophoresis
Laboratory findings
- Anemia , mostly due to impaired production of erythropoietin by kidneys. or GI bleeding.
- Eosinophilia is usually seen in patients with Churg-Strauss disease.
- Patients with RPGN may show formation of immune complexes and cryoglobulins.
- Complement C3 levels is usually low in immune-complex mediated RPGN.
- The presence of ANCA and anti-GBM is variable.
- ANCA-associated glomerulonephritis have high levels of ANCA, it is associated with disease activity.[1][2][3]
Urine Work-Up
- Urinalysis
- Urinary protein electrophoresis
- Patients with RPGN do not usually have a full-blown picture of nephrotic syndrome; Nephrotic syndrome only occurs in less than 30% of cases.[4]
- Proteinuria, if present, is usually mild to moderate. Hematuria of glomerular type with dysmorphic red blood cells is usually present on urinalysis and associated with red cell casts.
- Mild to moderate leukocyturia may be seen and other casts, such as epithelial cell leukocyte, or fatty casts. Urinary findings in RPGN are important features that not only favor diagnostic work-up, but also follow-up and therapeutic effectiveness.
References
- ↑ van der Woude FJ, Rasmussen N, Lobatto S, Wiik A, Permin H, van Es LA; et al. (1985). "Autoantibodies against neutrophils and monocytes: tool for diagnosis and marker of disease activity in Wegener's granulomatosis". Lancet. 1 (8426): 425–9. PMID 2857806.
- ↑ Tervaert JW, van der Woude FJ, Fauci AS, Ambrus JL, Velosa J, Keane WF; et al. (1989). "Association between active Wegener's granulomatosis and anticytoplasmic antibodies". Arch Intern Med. 149 (11): 2461–5. PMID 2684074.
- ↑ Falk RJ, Hogan S, Carey TS, Jennette JC (1990). "Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network". Ann Intern Med. 113 (9): 656–63. PMID 2221646.
- ↑ Hricik DE, Chung-Park M, Sedor JR (1998). "Glomerulonephritis". N Engl J Med. 339 (13): 888–99. doi:10.1056/NEJM199809243391306. PMID 9744974.