Acute Coronary syndrome VS Nonspecific Troponin Elevation

Acute Coronary syndrome VS Nonspecific Troponin Elevationvegetables at home Admission date : 96.9.5
Chief Complaint :
Refer from nephro OPD due to hyperkalemia and aggrvated nausea/vomiting for 1 month
Present Illness Chronic kidney disease, stage V found since 96/5
No D.M. nor HTN
96/3 96/5
96/9
Present Illness Progressive sharp pain over posterior neck to bil. arm and forearm, and right hip, right posterior thigh and leg Pain and weakness mad her hardly get up from bed ↓U.O. and urination frequency
Present Illness Neurologic exam: negative finding Lab exam: 7/11
BCS Albumin:4.0
BUN/Cr:60/8.2 HbA1C:6.5
Ca:10.0 P:6.2
RBC:1.99 M PLT:276 K WBC:6100 Seg:70%
Lymph:21% Band:1 %
Monocyte:8 %
Present Illness Color Pale yellow Turbidity Clear Sp.Gravity 1.010 PH 6.0 Leukocyte 1+ Nitrite Negative Protein 25 Glucose Negative Ketone Negative Urobilinogen 0.1
RBC 3 WBC 69
Blood 1+ Bacteria Positive
Stool OB: ( - )
Present Illness C-spine A-P view: 7/11 Cervical spondylosis Narrow disk spaces at C3-4 to C6-7 disk Osteoporosis
Present Illness Blood transfusion general weakness improved Consult nephro
Renal echo 24 hr Ccr: Ccr:5.4cc/min , UOP:1850
Left kidney length:10.2cm Right kidney length:10.4 cm
The cortical echogenicity is increased with adequate thickness The pelvocalyceal systems are not dilated
No obvious evidence of renal stone,mass or cyst Impression:Parenchymal renal disease
Present Illness
OPD F/U Discharge medications:
MgO 1# PO QID Cefadroxil (500mg) 2# QD X 7 days
Present Illness
96/3 96/5
Admission to Nephro
Present Illness Anorexia, Nausea/vomiting since 96/7, aggravating Tarry stool 1 week ago x 1 time No fever No dyspnea No abdominal discomfort
Personal history
Family history
Laboratory Findings 96/9/5
ColorColor yellow
TurbidityTurbidity Clear
trace / 7
EpithEpith--cellcell 3
Impression
74 y/o female Acute on chronic renal failure in uremic stage Hypercalcemia Normocytic anemia Chronic kidney disease stage V Bone pain Gastric ulcer in 96/5
Questions
What is the cause of renal failure ? What is the cause of hypercalcemia ? What is the cause of proteinuria ?
Questions 1: cause of RF
Prerenal? EAV ↓ or sepsis or drug or contrast or cyclosporine, tacrolimus
Postrenal Lower urinary tract obstruction Upper urinary tract obstruction Micro-obstructive uropathy
Intrinsic ? 9/5 BUN/Cr : 95/12.6 9/6 Urine specific gravity: 1.011 < 1.015
ATN Ischemic Toxic
AGN Nephrotic or nephritic syndrome
Vascular Thromboembolism Malignant hypertension Renal artery stenosis HUS/TTP
Lab: 9/7
RPR Negative Negative ANA Negative 1:80 C3 88.9 90~180 C4 56 10~40 IgG 570 700~1600 IgA <21.80 70~400 IgM <16.10 40~230 IgE 28.40 <100
Lab:
Questions 2: cause of Ca↑
Serum Ca level
Vit D deficiency 1’ hyperparathyroidism
Questions 3: proteinuria 9/6 U/A urine protein: 25 mg/dL 8/1 24hr Urine T.P.:1.6 g/day
Questions 3: proteinuria
Standard urine dipstick Primary detect albumin Insensitive to light chains + only when daily urine protein > 300 mg/day
SSA test( sulfosalicylic acid ) 1 part urine supernatant + 3 part 3% SSA Turbidity related to protein amount Detect all protein in the urine
Questions 3: proteinuria Category Description Etiologies
Isolated Asymptomatic,normal RFT,Urine sediments and
imaging
Nephrotic or nephritic syndrome
ATN AIN
Multiple myeloma Myoglobinuria
Impressions
Hospital course
9/10
Lab:Serum PEP/IFE 9/10
T.P. 5.70 gm/dL 6.3-8.0 Albumin 3.6 (63.6 %) gm/dL 3.2-5.5 A-1 globulin 0.2 (3.8%) 0.1-0.3 A-2 globulin 0.8 (13.3%) 0.6-1.0 Beta- globulin 0.6 (10.3%) 0.7-1.1 Gamma- globulin 0.5 (9.0%) 0.8-1.6 A/G 1.74 Comment Faint band at γregion
IFE Kappa-light chain (+)
Serum IFE
Hospital course
9/10
9/14
Lab:Urine PEP/IFE 9/13 mg/dL T.P.(U) 401.40 Albumin 32.50 (8.10 %) A-1 globulin 36.90 (3.8%) A-2 globulin 54.20 (13.50%) Beta- globulin 48.60 (12.10%) Gamma- globulin 229.20 ( 57.10%) A/G 0.08 Comment Monoclonal gammopathy pattern with two
spikes at γ region
Metastatic bone survey
Skull view T-L spine + L-S spine lateral view Humerus A-P + lateral view Femur A-P + lateral view
Hospital course
9/10
B.M. biopsy
9/14: 48276 μg/L : 1900 μg/L
Bone marrow biopsy Final Report: Multiple myeloma Site: Iliac :posterior , Right Microscopic findings:
Cellularity: 10-20% Megakaryocyte distribution: decreased markedly, morphology: Normal M/E ratio: 2.6 / 1 (myeloid series: 40.5 % of TNC), morphology: Normal Erythroid series: 15.6 % of TNC, morphology: normal Plasma cells : abnormal, ( 25.9 % of TNC), morphology abnormal myeloma cells
Discussion
Monoclonal gammopathy Multiple myeloma D.D of mutiple myeoma Renal failure in M.M. Treatment of renal failure in M.M.
Monoclonal gammopathies
Monoclonal gammopathies paraproteinemia dysproteinemia
Proliferation of a single clone of plasma cells which produce an immunologically homogeneous protein M-protein monoclonal protein
Plasma cell disorder Monoclonal gammopathy of undetermined significance (MGUS) POEMS syndrome, Osteosclerotic myeloma Castleman's disease AL (light chain) amyloidosis Solitary plasmacytoma Multiple myeloma, Smoldering multiple myeloma
B-cell lymphoproliferative disorders Non-Hodgkin's lymphoma Chronic lymphocytic leukemia Lymphoplasmacytic lymphoma (Waldenstrom macroglobulinemia)
Connective tissue disorders Systemic lupus erythematosus Rheumatoid arthritis
Associated with infections Hepatitis C virus infection ; HIV/AIDS
Dermatologic disorders: Scleroderma Miscellaneous disorders: Cryoglobulinemia
Monoclonal gammopathies
Blood 2006; 108:2520
↑ ESR or serum viscosity Unexplained anemia, back pain, weakness, or fatigue Osteopenia, osteolytic lesions, or spontaneous fractures Renal insufficiency with a bland urine sediment Heavy proteinuria in a patient over age 40 Hypercalcemia Hypergammaglobulinemia Immunoglobulin deficiency Bence Jones proteinuria Unexplained peripheral neuropathy Recurrent infections
Br J Haematol 2003; 121:749
Serum PEP:monoclonal gammapathy
α1 α2 β
SPEP: False (-) or (+)
False negative: M-protein complexes with other plasma components, or form IgM dimers and pentamers, IgA polymers, or IgG aggregates
False positive: Nephrotic syndrome often associated with increased alpha-2 and beta bands
Serum immunofixation
Serum IFE
Serum IFE indication
A sharp band or peak found in the agarose gel Suspect disease associated with monoclonal gammopathy with normal SPEP Document complete response to therapy that has resulted in disappearance of the band on routine PEP
24-hr urine collection for PEP and IFE
Indication Serum M-protein conc. > 1.5 g/dL or Diagnosis or clinical suspicion of plasma cell dyscrasia
Purpose Detect monoclonal light-chain disease Total amount of M-protein excreted in urine/day ( g/day)
Sensitive to detect M-rotein(U)0.004g/dL
Mayo Clin Proc 2003; 78:21.
Urine PEP/IFE of pt
Two discrete bands with either kappa or lambda antisera (but not both) usually due to the presence of monomers and dimers of the monoclonal light chain protein
Discussion
Monoclonal Monoclonal gammopathygammopathy Multiple myeloma
Definition of M.M A disorder in which malignant plasma cells accumulate, generally derived from one clone in the bone marrow Interactions between B.M.microenvironment and myeloma cells, frequently causing bone destruction, which in turn stimulates tumor growth. The tumor, its products, and the host response result in the multitude of symptoms and organ dysfunction characteristic of myeloma
THE LANCET • Vol 363 • March 13, 2004
Monoclonal (M) proteins
Monoclonal (M)- protein in the serum and/or urine in 97% of pts 20 % with no localized band on SPEP, hypogammaglobulinemia in ~ 1/2 of pts
N Engl J Med 351:1860, October 28, 2004
ETIOLOGY
The cause of multiple myeloma is unknown Exposure to radiation, benzene, and other organic solvents, herbicides, and insecticides may play a role Dr. : farmer has increased incidence
Epidemiology
~ 1 % of all malignant disease and ~ 10 % of hematologic malignancies in the US Annual incidence: 4 per 100,000 people Slightly more in men than in women The median age at diagnosis was 66 years Dr.: 1.41 per 100,000 people in 2003
in Taiwan
Common complaints
Bone pain: ~ 60% at the time of diagnosis Weakness and fatigue: 32 % and often associated with anemia Fever: < 1% BWL: 24 %
Mayo Clin Proc 2003; 78:21
Physical findings
Neurologic disease
Cord compression: ~ 5%, medical emergency Peripheral neuropathy: uncommon, usually due to amyloidosis; an exception is POEMS syndrome
CNS involvement Intracranial plasmacytomas: rare and skull lesion almost always (+) Encephalopathy: rare, due to
Hyperviscosity High blood ammonia level
Other findings
Incidence of infection: ↑,esp. to Strepto. pneumonia and GNB
Prone to infection due to Suppression of normal plasma cell function During chemotherapy During treatment with corticosteroid
Bone disease Conventional radiographs: 80% pt with lytic lesion at time of diagnosis Focal lytic lesions : 60 %
Osteoporosis: ~20% Pathologic fractures: ~20% Compression fractures of the spine: ~20%
Hypercalcemia : 28% ; Ca > 11 mg/dL in 13%
Mechanism of bone disease
Myeloma cells adjacent to bone produce various cytokines to cause
Stimulation of osteoclastic activity Inhibition of osteoblastic activity
Mechanism of bone disease Stimulation of osteoclastic activity
RANKL = osteoclast differentiation factor Cytokins with OAF activity : osteoclast activating function (OAF) : (IL-6, IL-11, IL-1b, TNFs, bFGF)
Inhibition of osteoblastic activity DKK-1 by myeloma cells inhibit osteoblast formation Cell-to-cell contact with the involvement of VLA-4–VCAM-1 interaction
Ann Oncol 2005; 16:1223
Skeletal surveys: skull, thoracic cage, vertebra bodies, pelvis, proximal humerus and femur CT and MRI :
helpful when pt has bone pain but no abnormalities on routine X-Ray MRI has significantly higher detection of focal lesions in the spine, pelvis, and sternum, while bone surveys outperformed MRI for lesions in the ribs and long bones
Renal disease
SCr at time of diagnosis : ↑~ 50% of pts 2 mg/dL in ~ 20 % of pts
Two major causes Cast nephropathy Hypercalcemia
Renal disease Primary amyloidosis: amyloid fibrils Light chain deposition disease: light chain fragments Radiocontrast media
CBC and blood smear
73 % at diagnosis 97 % at some time during the course
Rouleaux formation : 1/3 pts
Bone marrow exam of MGUS
M protein 1.5 gm/dL Non-IgG MGUS Abnormalities of the CBC, serum creatinine, serum calcium, or radiographic bone survey Abnormal serum free light chain ratio
Bone marrow examination
and prominent Golgi zones
B.M. exam: IgA M.M.
Bone marrow exam of M.M
Usually > 10 % plasma cells, but may range from < 5 % to almost 100 % May be more focal than diffuse
require B.M. aspirate/biopsy from several different sites
Immunoperoxidase staining confirms monoclonal plasma cell proliferation
Diagnosis criteria of M.M
International Myeloma Working Group WHO
The International Myeloma Working Group
Multiple Myeloma (all 3 criteria must be met) Presence of a serum or urinary monoclonal protein Presence of clonal plasma cells in the bone marrow or a plasmacytoma Presence of end organ damage felt related to the plasma cell dyscrasia, such as:
Increased calcium concentration Lytic bone lesions
Anemia, or
Renal failure
Asymptomatic (smoldering) multiple myeloma (SMM, both criteria must be met) Serum monoclonal protein 3 g/dL and/or bone marrow plasma cells 10 percent
No end organ damage related to plasma cell dyscrasia (see list above)
Monoclonal gammopathy of undetermined significance (MGUS, all 3 criteria must be met) Serum monoclonal protein <3 g/dL
Bone marrow plasma cells <10 percent No end organ damage related to plasma cell dyscrasia or a related B cell lymphoproliferative disorder
WHO criteria Major criteria (3) Bone marrow plasmacytosis >30 percent
Plasmacytoma on biopsy
Presence of a monoclonal protein (M-component) in serum or urine
Serum IgG >3.5 g/dL, or
Serum IgA >2 g/dL, or
Urine Bence-Jones protein >1g/24 hours
Minor criteria (4) Bone marrow plasmacytosis of 10 to 30 percent
Monoclonal protein present but less than the above concentrations
Presence of lytic bone lesions
Reduced normal immunoglobulins to <50 percent of normal
IgG <600 mg/dL, or
IgA <100 mg/dL, or
IgM <50 mg/dL
diagnosis requires a minimum of one major + one minor criterion, or three minor criteria
Durie-Salmon clinical staging system Stage Description
Low cell mass - <0.6 x 10(12) cells/m2
All of the following present:
Hgb >10 g/dL
No generalized lytic bone lesions
II Intermediate cell mass - neither stage I nor stage III
High cell mass - >1.2 x 10(12) cells/m2
One or more of the following:
Hgb < 8.5 g/dL
Advanced lytic bone lesions
B Serum creatinine 2 mg/dL
III
I
I B2M <3.5 mg/L and serum albumin 3.5 g/dL
II neither stage I nor stage III
III B2M 5.5 mg/L
I 62
II 44
III 29
Plasma cell cytogenetics
Deletion of 13q14: Significant ↓ in response rate to conventional C/T : 41% VS 79% Overall survival: 24 months VS 60 months
Hypodiploid A multivariate analysis of 208 pts with M.M The most significant factor adversely affect OS ( 12.5 months VS 33.8 months)
Blood 2000; 95:1925
Blood 2001; 98:2229
Chromosomal translocation in M.M
14q32 - the most commonly involved T ( 11; 14) (q13; q32) result in up-regulation of cyclin D1
Blood 1996; 88:674.
Cytogenetic testing 351 M.M pts treated with conventional C/T had FISH analysis
Poor prognosis group: MS:25 months t(4;14)(p16;q32) t(14;16)(q32;q23 -17p13 hypodiploidy
Intermediate prognosis: MS: 42 months -13q14
Good prognosis : MS: 50 months All others
Blood 2003; 101:4569
PCLI
Double immunoflorescence technique Fresh B.M. cells incubated in vitro A fluorescent monoclonal Ab identifies cells that synthesize DNA Use in pt with stable, plateu phase M.M
Blood 2001; 97:2522.
ISS Cytogenetic testing Circulating plasma cells Plasma cell labeling index ( PCLI)
D.D. of multiple myeloma
Monoclonal gammopathy of undetermined significance
Serum M component < 3g/dL B.M. plasma cells < 10% Absence of ROTI (related organ tissue injury) Progression to M.M or related malignancy ~ 1 % / year
N Engl J Med 2002; 346:564
Smoldering multiple myeloma
M-protein >3 g/dL and/or 10 % bone marrow plasma cells Absence of ROTI (related organ tissue injury) Progression to myeloma > 3.3 % / year
Primary amyloidosis
Clinical manifestations different Tissue deposits of amyloid fibril or non- fibrillar material that produce
Nephrotic syndrome Heart failure Hepatomegaly
Usually no lytic bone lesion Diagnosis by biopsy of affected tissue
Nephrotic syndrome+ urine FLC
Arch Pathol Lab Med 1999; 123:114
Metastatic cancer
Lytic bone lesion with small M component,<10% plasma cells in B.M.+ constitutional symptoms Lytic bone lesion without M-protein in serum or urine exclude Metastatic Ca. before consider non-secretory myeloma
Primary bone response to some tumors
Predominantly osteolytic Renal cell cancer Melanoma Squamous cell cancers of the aerodigestive tract Non-small cell lung cancer
Thyroid cancer Non Hodgkins lymphoma Multiple myeloma
Mixed osteoblastic and osteolytic Breast cancer Gastrointestinal cancers Squamous cancers at most primary sites
Type of monoclonal protein in M.M Serum IgG : 51.5 % IgA : 21 % Light chain : 16 % ( κ/λ~ 2/1 ) IgD : 2 % Biclonal : 2 % IgM: 0.5 % No monoclonal protein:7 %
Mayo Clin Proc 2003; 78:21
Light chain myeloma
Only a light chain in the serum or urine ~ 16 % of myeloma The incidence of renal failure : higher Serum creatinine 2 mg/dL in about 1/3 of pts at presentation
Light chain myeloma
Supportive measures to minimize renal damage (eg, avoidance of aminoglycosides and NSAIDs, maintenance of hydration) are warranted in any myeloma patient with urinary free light chain excretion
Renal disease in M.M. Monoclonl Ig light chain related
Myeloma cast nephropathy Primary amyloidosis Light chain deposition disease Renal tubular dysfunction
Nephrol Dial Transplant 1998; 13:1438.
Renal disease in M.M.
Acute myeloma kidney. Kidney Int 1995; 48:1347
Renal disease in M.M.
Only one type of light chain renal disease is clinically manifested in one pt
Am J Kidney Dis 1983; 2:423.
Myeloma cast nephropathy
Acute or chronic RF due to filtration of toxic light chain, leading to
Tubular injury Intratubular cast formation and obstruction
Binding of light chain to Tamm-Horsfall mucoprotein
Myeloma cast nephropathy
Slowing flow within the tubules Increasing the light chain conc.
Loop diuretics: ↑ luminal NaCl conc. ↑ light chain aggregate with THMP
Myeloma kidney
Diagnosis definitively made with a kidney biopsy Often established by:
ARF + large amount of monoclonal free light chain in the serum / urine
Cast nephropathy in M.M
Reabsorption of filtered light chains Subsequent accumulation in the proximal cells
Part of variable domain is resistant to degradation by proteases in lysosomes in the tubular cells
intracellular crystal formation
Lab finding Hypouricemia ( in the absence of allopurinol )
Other causes of ARF Hypercalcemia cause RF by
Renal vasoconstriction Intratubular Calcium deposition Concentration defect due to impairment of
NaCl reabsorption in the thick ascending limb ADH resistance
Concentrating defect become clinically apparent when plasma Ca persistently > 11 mg/dL Renal failure and ADH resistance caused by hypercalcemia are generally reversible by correction of hypercalcemia
Kidney Int 1987; 31:1065..
Other causes of ARF
IV radiocontrast < 1.5 % in M.M. Hydration before study likely to be protective
NSAID Should be avoided as possible
Hyperuricemia ~ 50% with M.M.
Renal failure in M.M.
An increase in serum Cr conc. to 2.0mg/ dL ( 177 μmole/L) ~ 20% of pts with M.M. at presentation
Arch Intern Med 1998; 158:1889. .
Early mortality in pt with M.M.
Clin Oncol 23:9219-9226. © 2005
Prevention Acute renal failure
Specific treatment directed at the cause Chronic renal failure ESRD
Treatment of ARF in M.M.
Myeloma cast nephropathy Receive chemotherapy as rapidly as possible to decrease light chain production
Volume depletion, hypercalcemia and hyperuricemia
Vigorous IV fluid therapy unless contraindicated: goals Decrease light chain concentration within the tubular lumen Decrease NaCl conc, in the tubular fluid Produce high urine flow rate to minimize light chain precipitation
Vigorous IV fluid regimen Isotonic / half isotonic saline at initial rate of 150 ml/hr, +- to keep U.O.P. ~ 100 to 150 ml/hr ( 3000 ml/ day ) Require careful monitoring ( CVP ) especially in pt with HF or oliguric/anuria ARF No RCT of loop diuretics to help guide therapy Fluid regimen x 24 hrs in pt with oliguric ARF
Guidelines on the diagnosis and management of multiple myeloma 2005. Br J Haematol 2006
Tx of hypercalcemia in M.M.
Based on initial corrected serum Ca conc. Serum Ca < 14 mg/dL ( 4 mmol/L)
Fluid regimen first If hypercalcemia persists 6~12 hrs later bisphosphonate
Serum Ca 14 mg/dL Bisphosphonate immediately + concurrent fluid regimen
Tx of hypercalcemia in M.M. Dose adjustment of bisphosphonates in renal failure The manufacturers’ guidance :
Clodronate: half dose if Ccr: 10–30 ml/min; contraindicated if <10 ml/min; Pamidronate: slower infusion rate (20 mg/h) if renal impairment; Zometa:check creatinine before each infusion,ensure hydration; not recommended if serum Cr >265 μmole/L ( 3 mg/ dL )
Tx of hyperuricemia in M.M.
( Uricase, Rasburicase )
Stop NSAIDs,ACEI or AIIB Avoid radiocontrast dye
Dialysis initiated as necessary PD HD : preferred due to doubled use
If plasmapheresis use citrate anticoagulation Dialysis post plasmaphoresis to correct alkalemia
Plasmapheresis in pts with acute renal failure due to myeloma : evidence conflicting
Controlled plasma exchange trial in acute renal failure due to multiple myeloma. Kidney Int 1988; 33:1175. Plasma exchange when myeloma presents as acute renal failure: a randomized, controlled trial. Ann Intern Med 2005; 143:777.
Kidney Int 1988; 33:1175
Conclusion: plasma exchange associated to chemotherapy
rapidly removes large amounts of light chains improves renal function improves long-term survival expectancies
Ann Intern Med 2005; 143:777
Unadjusted Odds ratio(95% CI) Adjusted Odds ratio(95% CI)
Shortcomings of the 2nd one Free light chain M.M. only 76 out of 97 pts Plasmapheresis associated with a 52% reduction in dialysis dependence among survivors at 6 months (13 % VS 27%)
Indication for plasmapheresis Acute renal failure suspected to be due to cast nephropathy Pt with cast nephropathy on kidney biopsy May be initiated based on high level of free monoclonal light chains in the serum or urine
Protocol 5~7 exchanges within 7~ 10 days Plasmapheresis + dexamethasone-containing C/T to ↓ rate of light chain production Repeat monoclonal light chain assay to monitor recurrent light chain accumulation 1~2 days after completing the initial course Prolong or repeat the course may be reasonable
ARF due to hypercalcemia and volume depletion are most likely to recover Those with dense cast formation and significant tubular damage are less likely to recover kidney function
Renal failure in multiple myeloma Arch Intern Med 1990; 150:1693
Tx of CRF in M.M.
Insufficient evidence of benefit from plasmapheresis in pts with chronic,slowly progressive renal failure Generally suggest chemotherapy alone to reduce light chain production
Tx of ESRD in M.M.
H/D or PD Actual survival: 45 % at 1 year, 25% at 2 year C/T responsive ( MS: 47 months) VS 17 months in nonresponder
Prevention
Light chain filtration Tubular obstruction
Fluid therapy Dexamethasone-based chemotherapy Aoid nephrotoxins
C/T in M.M.
Thanks for your attention
Serum viscosity
Monoclonal gammopathy and symptoms /signs suggesting hyperviscosity syndrome Monoclonal IgM protein spike is >4 g/dL or the IgA or IgG protein spike is >6 g/dL.
J Intensive Care Med 1995; 10:128
Serum viscosity
Relative viscosity to water Normal serum viscosity:1.4~2.0 Symptoms of hyperviscosity usually occur at level of 5~6, roughly equals
IgM: 4 g/dL IgG3: 5 g/dL IgA : 7 g/dL
Hypogammaglobulinemia
γ globulin <0.6 g/dL a decrease in size of the gamma mobility component on SPEP occurs in ~10 % pts with M.M Most of them have a Bence Jones protein in the urine, but lack intact immunoglobulins in the serum
Arch Pathol Lab Med 1999; 123:114
Serum free light chains immunoassay
Monoclonal light-chain diseases Light-chain myeloma (Bence Jones protein MM) Primary systemic amyloidosis (AL) Light-chain-deposition disease (LCDD)
Nonsecretory myeloma (NSMM)
Lancet 2003; 361:489
FLC assay VS urine PEP
Comparison: Urine is a poor medium for testing 24-h urine collections may be difficult to obtain from elderly frail individuals
Conclusions: Serum assays could replace Bence Jones protein urine tests for pts with light-chain multiple myeloma
Lancet 2003; 361:489
Nephro Case Conference
Lab: 9/7
Lab:
Urine PEP/IFE of pt
Bone marrow examination
Diagnosis criteria of M.M
WHO criteria
Smoldering multiple myeloma
Light chain myeloma
Light chain myeloma
Tx of hyperuricemia in M.M.
Tx of CRF in M.M.
Tx of ESRD in M.M.
Prevention

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Acute Coronary syndrome VS Nonspecific Troponin Elevation