This document discusses lupus nephritis, including its pathophysiology, risk factors, clinical presentation, investigations, classification, treatment, and prognosis. Key points include:
- Lupus nephritis is a serious manifestation of systemic lupus erythematosus caused by autoantibodies forming immune complexes that deposit in the glomeruli.
- It is classified based on renal biopsy findings, with classes III and IV having the highest risk of progressing to end-stage renal disease.
- Treatment involves immunosuppressive induction therapy with corticosteroids and cyclophosphamide or mycophenolate mofetil to rapidly decrease inflammation, followed by long-term maintenance
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
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lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
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Systemic lupus erythematosus (SLE) is the prototypic multisystem autoimmune disorder with a broad spectrum of clinical presentations encompassing almost all organs and tissues.
The extreme heterogeneity of the disease has led some investigators to propose that SLE represents a syndrome rather than a single disease.
Lupus was first recognised as a systemic disease with visceral manifestations by Moriz Kaposi (1837–1902).
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
2. In 1941, Klemperer, Pollack and Baehr first
described systemic lupus erythematosus (SLE)
as one of the Connective Tissue Disease.
19th-
century
• The term “lupus
erythematosus” was
introduced to describe skin
lesions
almost
100 years
later
• the disease is systemic and
spares no organ
3. SYSTEMIC LUPUS ERYTHEMATOSUS
Systemic lupus erythematosus is an
autoimmune disease in which organs and
cells undergo damage initially mediated by
tissue binding autoantibodies and immune
complexes.
4. LUPUS NEPHRITIS
• Lupus nephritis is histologically evident in most
patients with SLE.
• One of the most serious manifestations of SLE.
• Usually arises within 5 years of diagnosis.
5. PATHOPHYSIOLOGY
Autoimmunity plays a major role in the
pathogenesis of lupus nephritis.
Immunologic
mechanisms
Production of
autoantibodies
Against nuclear
elements
6. The characteristics of the nephritogenic autoantibodies
associated with lupus nephritis are as follows :
i. Antigen specificity directed against nucleosome or double-
stranded DNA (dsDNA) - Some anti-dsDNA antibodies cross-
react with the glomerular basement membrane.
ii. Higher-affinity autoantibodies may form intravascular
immune complexes, which are deposited in glomeruli.
iii. Cationic autoantibodies have a higher affinity for the anionic
glomerular basement membrane.
iv. Autoantibodies of certain isotypes (immunoglobulin IgG 1 and
IgG 3) readily activate complement.
7. Autoantibodies
Form pathogenic immune
complexes intravascularly
Immune complexes
deposited in glomeruli
Bind to antigens already
located in the glomerular
basement membrane
Immune complexes in situ
Activating complement and attracting inflammatory cells, including
lymphocytes, macrophages, and neutrophils
Promote an inflammatory
response
The histologic type of lupus nephritis that develops depends on
numerous factors, including the antigen specificity and other
properties of the autoantibodies and the type of inflammatory
response that is determined by other host factors.
8. ETIOLOGY
There are multiple susceptibility factors, which
result in abnormal immune responses, which vary
among different patients.
These factors include:
• Genetic factors
• Immunologic factors
• Environmental factors
9. GENETIC FACTORS
Genetic predisposition plays an important role in the development
of both SLE and lupus nephritis. Multiple genes, many of which are
not yet identified, mediate this genetic predisposition [Human
leukocyte antigen (HLA) class II genes, Complement genes, FcγR
genes and others]
10. IMMUNOLOGIC FACTORS
• Patients with SLE have poor clearance mechanisms for
cellular debris. Nuclear debris from apoptotic cells induces
plasmacytoid dendritic cells to produce interferon-α, which
is a potent inducer of the immune system and
autoimmunity.
• Autoreactive B lymphocytes, which are normally inactive,
become active in SLE because of a malfunction of normal
homeostatic mechanisms, resulting in escape from
tolerance. This leads to the production of autoantibodies.
• Anti-dsDNA antibodies, develop through a process of
epitope spreading.
12. EPIDEMIOLOGY
50–60% developing nephritis during the first
10 years of disease.
35% adults having SLE have clinical
evidence of nephritis at time of diagnosis.
African Americans and
Hispanics
Whites
14. BANGLADESH
Lupus nephritis was the most prevalent
among secondary GN
common histological type
was found Class IV [40%]
Female 73.2% 21-40
year age
ANA positive
63%
Anti-ds DNA
was positive
100%
15. CLINICAL FEATURES: SYMPTOMS
1. Asymptomatic
2. Symptoms of active systemic lupus erythematosus (SLE),
including fatigue, fever, rash, arthritis, serositis, or central
nervous system (CNS) disease.
3. Symptoms related to active nephritis may include peripheral
edema secondary to hypertension or hypoalbuminemia.
4. Other symptoms directly related to hypertension that are
commonly associated with diffuse lupus nephritis include
headache, dizziness, visual disturbances, and signs of cardiac
decompensation.
16. • Focal and diffuse lupus nephritis: evidence of
generalized active SLE with the presence of a rash, oral
or nasal ulcers, synovitis, or serositis. Signs of active
nephritis are also common.
• Active lupus nephritis: hypertension, peripheral edema,
and, occasionally, cardiac decompensation.
• Membranous lupus nephritis: signs of an isolated
nephrotic syndrome are common. These include
peripheral edema, ascites, and pleural and pericardial
effusions without hypertension.
CLINICAL FEATURES: SIGNS
17. • Several studies have focused on the
discrepancy between clinical presentation
and pathologic findings at renal biopsy in
patients with SLE.
• Silent LN has been reported not only in
class II but also in class IV.
• Even patients with low-level proteinuria
(<1g/24h) have demonstrated significant
renal involvement with proliferative LN
(classes III or IV).
20. INVESTIGATIONS:
Evaluating renal function
• To detect any renal involvement early.
Renal biopsy
• Classification is based on light microscopy,
immunofluorescence, and electron microscopy
findings from renal biopsy specimens.
21. LABORATORY TESTS
• Blood urea nitrogen (BUN)
• Serum creatinine
• Urine R/M/E (to check for protein, red blood cells [RBCs],
and cellular casts)
• A spot urine test for creatinine and protein concentration
(normal creatinine excretion is 1000 mg/24 h/1.75 m 2;
normal protein excretion is 150-200 mg/24 h/1.75 m 2;
normal urinary protein-to-creatinine ratio is <0.2)
• A 24-hour urine test for creatinine clearance and protein
excretion
22. • ANA [for diagnosis SLE]
• Antibodies to double-stranded DNA (dsDNA), ↑
• Complement (C3, C4, and CH50), ↓
• Erythrocyte sedimentation rate (ESR), ↑
• C-reactive protein (CRP) levels. ↔
• Anti-C1q antibodies ↑ [less sensitive then Anti
dsDNA, but more specific]
LABORATORY TESTS
23. Urinary biomarkers can accurately identify active
lupus nephritis in children:
• Alpha-1-acid glycoprotein (AGP)
• Ceruloplasmin
• Lipocalin-like prostaglandin D synthase (LPGDS)
• Transferrin
LABORATORY TESTS
25. ACR CRITERIA
ACR criteria
Persistent proteinuria >0.5
gm per day or greater than
3+ by dipstick, and/or
Cellular casts including red
blood cells [RBCs],
hemoglobin, granular,
tubular, or mixed
Review of the
ACR criteria
Spot urine
protein/creatinine ratio of
>0.5
Active urinary sediment (>5
RBCs/HPF, >5 WBCs/HPF in
the absence of infection, or
cellular casts limited to RBC
or WBC casts
26. RENAL BIOPSY
All patients with clinical evidence of active LN,
previously untreated, undergo renal biopsy (unless
strongly contraindicated) for
• Classified by current ISN/RPS classification
• Disease evaluated for activity and chronicity
• Identify additional or alternative causes of renal
disease
• Determining prognosis and treatment
27. INDICATIONS FOR RENAL BIOPSY IN PATIENTS
WITH SYSTEMIC LUPUS ERYTHEMATOSUS
• Increasing serum creatinine without compelling alternative
causes (such as sepsis, hypovolemia, or medication)
• Confirmed proteinuria of 1.0 gm per 24 hours (either 24-
hour urine specimens or spot protein/creatinine ratios are
acceptable)
• Combinations of the following, assuming the findings are
confirmed in at least 2 tests done within a short period of
time and in the absence of alternative causes:
• Proteinuria 0.5 gm per 24 hours plus hematuria,
defined as 5 RBCs per hpf
• Proteinuria 0.5 gm per 24 hours plus cellular casts
28. International Society of Nephrology/Renal Pathology Society 2003 classification
of LN
Class I Minimal mesangial LN
Class II Mesangial proliferative LN
Class III Focal LN (50% of glomeruli)
III (A): active lesions
III (A/C): active and chronic lesions
III (C): chronic lesions
Class IV Diffuse LN (50% glomeruli)
Diffuse segmental (IV-S) or global (IV-G)
LN
IV (A): active lesions
IV (A/C): active and chronic lesions
IV (C): chronic lesions
Class V Membranous LN
Class VI Advanced sclerosing LN (90% globally
sclerosed glomeruli without residual
activity)
30. CLASS II
Mesangial cell proliferation,
mesangial matrix expansion.
Granular mesangial positivity of all three
immunoglobulins and both
complements (C1q and C3) (“full house”
pattern)
31. CLASS III
Less than 50% of all glomeruli,
segmental or global, swelling and
proliferation of endothelial and
mesangial cells associated with
leukocyte accumulation, capillary
necrosis, and hyaline thrombi;
extracapillary proliferation,
crescents.
Full house pattern as in class II,
immune deposits also identified in
tubular basement membranes,
interstitial capillary walls,
interstitial collagen, arterial intima,
and media, Fibrinogen positivity
35. CLASS V
Diffuse thickening of the capillary
walls due to deposition of
subepithelial immune complexes,
increased production of basement
membrane-like material
There are delicate subepithelial
immune deposits staining for IgG
with or without mesangial deposits
36. CLASS VI
Sclerosis of more than 90% of the
glomeruli, end stage renal disease, severe
tubular atrophy, interstitial fibrosis,
inflammation.
38. TREATMENT
The principal goal of therapy in lupus nephritis is to normalize
renal function or, at least, to prevent the progressive loss of renal
function. Therapy differs depending on the pathologic lesion.It is
important to treat extrarenal manifestations and other variables
that may affect the kidneys.
• Adjunctive Treatments
• Primary disease management by immunosuppressive agents
• Induction Therapy
• Maintenance Therapy
• Lifestyle Changes
39. ADJUNCTIVE TREATMENTS
Drugs Cause
Hydroxychloroquine
[Max 6–6.5 mg/kg body weight]
All SLE patients with; unless there is a
contraindication:
• Lower rates of Flare
• Reduced renal damage
• Less clotting events
ACEi/ARBs Patients with proteinuria >0.5 gm/day
• Reduces proteinuria by 30%, and
• Significantly delays doubling of serum
creatinine
• Delays progression to ESRD
Antihypertensive Target of ≤130/80 mmHg
• Significant delay in progression of
renal disease
Statin therapy Patients with LDL >100 mg/dl
• As GFR<60ml/min/1.73m2 & SLE itself
accelerated atherosclerosis
Calcium supplementation Prevent osteoporosis if the patient is on
long-term corticosteroid therapy
40. IMMUNOSUPPRESSIVE AGENTS
• Depends upon class of LN diagnosed on kidney
biopsy along with presence of extra-renal
manifestations of SLE
• Goals of immunosuppressive treatment:
• Long-term preservation of renal function,
• Prevention of flares,
• Avoidance of treatment-related harms, and
• Improved quality of life and survival.
41. CLASS I LN (MINIMAL-MESANGIAL LN)
Treatment as dictated by the extrarenal clinical
manifestations of lupus
• Class I LN has no clinical kidney manifestations.
• Class I LN is not associated with long-term
impairment of kidney function
42. • May require treatment if proteinuria is
greater than 1000 mg/day.
• Consider prednisone in low-to-moderate
doses (ie, 20-40 mg/day) for 1-3 months,
with subsequent taper.
CLASS II LN (MESANGIAL-PROLIFERATIVE LN)
43. CLASS III LN (FOCAL) AND CLASS IV LN (DIFFUSE)
• At high risk of progressing to ESRD
• Require aggressive therapy.
• Therapy for class III and IV LN has 2 phases:
• Initial/Induction phase: to rapidly decrease kidney
inflammation
• Maintenance phase: to consolidate treatment over a
longer time.
45. INITIAL/INDUCTION PHASE
• Initial therapy with corticosteroids , combined with
either cyclophosphamide or MMF.
• If patients have worsening LN (rising SCr, worsening
proteinuria) during the first 3 months of treatment, a
change be made to an alternative recommended initial
therapy, or a repeat kidney biopsy be performed to
guide further treatment.
46. GLUCOCORTICOIDS
• Pulse IV glucocorticoids (500–1000 mg
methylprednisolone daily for 3 doses) in
combination with immunosuppressive therapy is
recommended.
• Followed by daily oral glucocorticoids (0.5–1
mg/kg/day), followed by a taper to the minimal
amount necessary to control disease.
47. REGIMENS FOR INITIAL THERAPY IN CLASS III/CLASS
IV LN [INTERNATIONAL SOCIETY OF NEPHROLOGY- KIDNEY DISEASE IMPROVING
GLOBAL OUTCOME]
48.
49. MMF CYC
• Non Asian = 3gm/D
• Asian = 2 gm/D
• Class III/IV + crescents = 3gm/D
• Proteinuria + recent significant
rise in creatinine = 3gm/D
• In severe class III/IV LN
• In whites, low- and high-dose regimens were
equivalent in efficacy.
• Serious infections were less frequent with the lower
doses
• Low and high-dose regimens similar rates of LN
flares, end-stage renal disease, and doubling of the
serum creatinine.
50. IMPORTANT CONSIDERATIONS FOR CYC
• The use of sodium-2-mercaptoethane (mesna) will also minimize the
risk of hemorrhagic cystitis when cyclophosphamide is given as i.v.
pulses.
• Lifetime maximum of 36 g cyclophosphamide in patients with
systemic lupus as there is chance of hematologic malignancies later
in life.
• The dose of cyclophosphamide should be decreased by 20% (CrCl
25-50ml/min) or 30% (10–25 ml/min)
• To minimize bladder toxicity with oral cyclophosphamide, suggest
instructing patients to take cyclophosphamide in the morning, and to
drink extra fluid.
• To protect fertility, women should be offered prophylaxis with
leuprolide and men testosterone. Ovarian tissue
cryopreservation/sperm banking are other options.
51. HOW CAN WE PREDICT OUTCOME??
• After 8 week: ≥ 25% reduction in proteinuria
and/or normalization of C3 and/or C4 serum
levels = likely to show good clinical renal
responses
• After 6 months: decrease in serum creatinine
and in proteinuria to <1 gm/D predicts a good
long-term outcome
52. DEFINITIONS OF RESPONSE TO THERAPY
• Complete response: Return of SCr to previous baseline, plus a
decline in the uPCR to <500 mg/g (<50 mg/mmol).
• Partial response: Stabilization (±25%), or improvement of SCr,
but not to normal, plus a ≥50% decrease in uPCR. If there was
nephrotic-range proteinuria (uPCR≥3000 mg/g [≥300
mg/mmol]), improvement requires a ≥50% reduction in uPCR,
and a uPCR <3000 mg/g [<300 mg/mmol].
• Deterioration: There is no definition of deterioration in LN to
define treatment failure. A sustained 25% increase in SCr is
widely used but has not been validated.
56. OTHER INITIAL REGIMENS
Regimens
Rituximab • When treatment failed with MMF/CYC
Azathioprine • 2nd line protocol
• Less effective than CYC
MPA • Less nausea & diarrhea than MMF
• Should measured 1 hour after a dose
Cyclosporine • (4–5 mg/ kg/d) was used for 9 months, and then
tapered over the next 9 months.
• No differences in responses, relapse rate, Infections and
leukopenia with CYC.
• ACR guideline preferred it for maintenance therapy.
Tacrolimus • Equivalent to high-dose IV CYC in inducing complete
and partial remissions of LN
60. • Azathioprine (1.5–2.5 mg/kg/d) or
• MMF (1–2 g/d in divided doses)
±
Low-dose oral corticosteroids
Calcineurin inhibitors with low-dose corticosteroids be
used for maintenance therapy in patients who are intolerant
of MMF and azathioprine.
MAINTENANCE THERAPY
61. Complete remission
is achieved
Repeat
kidney
biopsy
Change in
therapy
Continued for at
least 1 year
Consideration for
tapering
Kidney function
deteriorates and/or
proteinuria worsens
Treatment be increased
to the previous level of
immunosuppression
that controlled the LN
YESNO
After
1 year
62. DURATION OF THERAPY
• There is no evidence to help determine the
duration of maintenance therapy.
• The average duration of immunosuppression was
3.5 years in seven RCTs.
• Immunosuppressive therapy should usually be
slowly tapered after patients have been in
complete remission for a year.
63. CLASS V LN (MEMBRANOUS LN)
• Generally treated with prednisone for 1-3 months,
followed by tapering for 1-2 years if a response occurs. If
no response occurs, the drug is discontinued.
• Immunosuppressive drugs are generally not used unless
renal function worsens or a proliferative component is
present on renal biopsy samples.
64. CLASS VI LN (ADVANCED SCLEROSIS LN)
• Treated with corticosteroids and
immunosuppressives only as dictated by the
extrarenal manifestations of systemic lupus.
• Dialysis and
• Kidney transplantation
65. LIFESTYLE CHANGES FOR LUPUS NEPHRITIS
• Drink enough fluids to stay well hydrated.
• Eat a low-sodium diet, especially if hypertension is an
issue.
• Avoid smoking and drinking alcohol.
• Exercise regularly.
• Maintain a healthy blood pressure.
• Limit cholesterol.
• Avoid medications that can affect the kidneys, such as
nonsteroidal anti-inflammatory drugs (NSAIDs).
66. RELAPSE OF LN
• Treated with the initial therapy followed by the
maintenance therapy that was effective in
inducing the original remission
• Consider a repeat kidney biopsy during relapse if
there is suspicion that the histologic class of LN
has changed, or there is uncertainty whether a
rising SCr and/or worsening proteinuria
represents disease activity or chronicity.
67.
68. SYSTEMIC LUPUS AND THROMBOTIC
MICROANGIOPATHY
• Antiphospholipid syndrome occurs when immune
system mistakenly attacks some of the normal proteins
in blood.
• The antiphospholipid anti-body syndrome (APS)
involving the kidney in systemic lupus patients, with or
without LN.
69. Blood tests for antiphospholipid syndrome look for at least
one of the following three antibodies in your blood:
• Lupus anticoagulant
• Anti-cardiolipin
• Beta-2 glycoprotein I
To confirm a diagnosis of antiphospholipid syndrome, the
antibodies must appear in your blood at least twice, in tests
conducted at least 12 weeks apart.
SYSTEMIC LUPUS AND THROMBOTIC
MICROANGIOPATHY
70. • Heparin: Typically, first be given as injection, combined
with another blood thinner in pill form, likely warfarin
(Coumadin).
• Warfarin: After several days of combined heparin and
warfarin, discontinue the heparin and continue the
warfarin, possibly for the rest of life.
• Aspirin: In some cases, may recommend adding low-dose
aspirin to treatment plan.
Target INR 2–3
SYSTEMIC LUPUS AND THROMBOTIC
MICROANGIOPATHY
71. • Patients with systemic lupus and thrombotic
thrombocytopenic purpura (TTP) receive plasma
exchange as for patients with TTP without systemic
lupus.
SYSTEMIC LUPUS AND THROMBOTIC
MICROANGIOPATHY
72. SYSTEMIC LUPUS AND PREGNANCY
• Women be counseled to delay pregnancy until a
complete remission of LN has been achieved.
• In patients with prior LN but no current evidence of
systemic or renal disease activity: no nephritis
medications are necessary
• Patients with mild systemic activity: may be treated with
HCQ
• Clinically active nephritis is present, or there is substantial
extrarenal disease activity: glucocorticoids (at doses
necessary to control disease activity) ± AZA
73. • If pregnant patients are receiving corticosteroids or
azathioprine, we suggest that these drugs not be
tapered during pregnancy or for at least 3 months after
delivery.
• Contraindicated: High-dose glucocorticoid [hypertension
and diabetes mellitus]. MMF, CYC, and methotrexate
should be avoided because they are teratogenic.
• Class III or IV with crescents: consideration of delivery
after 28 weeks for a viable fetus.
• Administration of low-dose aspirin during pregnancy to
decrease the risk of fetal loss.
SYSTEMIC LUPUS AND PREGNANCY
Some patients have asymptomatic lupus nephritis; however, during regular follow-up, laboratory abnormalities such as elevated serum creatinine levels, low albumin levels, or urinary protein or sediment suggests active lupus nephritis. This is more typical of mesangial or membranous lupus nephritis.symptoms of active systemic lupus erythematosus (SLE), including fatigue, fever, rash, arthritis, serositis, or central nervous system (CNS) disease. These are more common with focal proliferative and diffuse proliferative lupus nephritisSymptoms related to active nephritis may include peripheral edema secondary to hypertension or hypoalbuminemia. Extreme peripheral edema is more common in persons with diffuse or membranous lupus nephritis, as these renal lesions are commonly associated with heavy proteinuria.
An additional, perhaps optimal, criterion is a renal biopsy sample demonstrating immune complex–mediated glomerulonephritis compatible with LN
Cellular crescents are a feature of active lupus nephritis.
Cellular crescents commonly overlie necrosis of the glomerular tuft, and are formed by proliferating parietal epithelial cells with infiltrating mononuclear cells (monocytes or macrophages).
The greater the proportion of glomerular involvement (i.e > 50%), the worse the prognosis.
With evolution of the glomerular injury, there is progressive scarring of cellular crescents, forming fibrocellular and fibrous crescents.
Wire loops, a classic sign of active lupus nephritis, are segmental areas of refractile, eosinophilic, thickening of the glomerular capillary seen by light microscopy in haematoxylin and eosin stained sections.
They correspond to massive subendothelial electron-dense deposits on electron microscopy, that when large enough to completely involve the peripheral circumference of the glomerular capillary wall.
Hyaline thrombi are large, acellular, eosinophilic, intracapillary deposits that occlude the glomerular capillary lumens
The term is actually a misnomer because they do not represent true fibrin thrombi but are instead massive intracapillary immune deposits