Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
122 Cards in this Set
- Front
- Back
|
how much protein is normal in a 24 hour urine?
|
no more than 150
|
|
|
early in diabetic Kidney disease what are the size of the kidney?
|
enlarged
|
|
|
Extrarenal hematuria
|
Urinary tract infections
Bladder cancer |
|
|
Non‐glomerular Renal hematuria
|
Cysts, stones, renal cancer, interstitial nephritis
|
|
|
Questions in the history of Non‐glomerular Hematuria
|
History of nephrolithiasis, urinary tract
infections, trauma, vigorous exercise, sickle cell anemia/trait • Abdominal pain, flank pain, colic pain • Family history of nephrolithiasis, vesicoureteral reflux, cystic kidney disease |
|
|
Non‐glomerular Hematuria
• Evaluation of urine: consists of |
– Red urine
– Uniform RBC’s – Clots, crystals – No significant proteinuria – No casts |
|
|
any casts or proteinuria in non glomerular hematuria
|
no no no
|
|
|
Glomerular Hematuria
• History |
• History of fever, malaise, rash, arthralgias, oliguria,
weight change • Recent upper respiratory infection or febrile illness • Recent throat or skin infection • History of other systemic diseases (systemic lupus erythematosis [SLE], vasculitis, Henoch purpura [HSP]) • Family history of renal failure, hematuria, hearing loss |
|
|
def of oliguria
|
less than 400cc
|
|
|
Glomerular Hematuria
• Evaluation of urine: consits of |
– Brown or tea colored
– Dipstick positive for blood and protein – Dysmorphic RBC’s – Cellular casts |
|
|
key urine finding in Glomerular hematuria
|
dysmorphic red cells
|
|
|
Dysmorphic red cells
|
key urine finding in Glomerular hematuria
|
|
|
Protein content determined by 3 factors
|
– Filtration of proteins present in plasma
immunoglobulins – Reabsorption of filtered protein – Tubular secretion of protein – albumin, – Tamm‐Horsfall |
|
|
In membranous
nephropathy what happens to one of the barrers to filtration |
Size – molecules with size > 150 kd (membranous
nephropathy) |
|
|
• Barriers to filtration
|
Size – molecules with size > 150 kd (membranous
nephropathy) – Charge – polyanionic glycosaminoglycans in the basement membrane provide a charge selective barrier (minimal change disease) – Albumin – restricted primarily by charge |
|
|
albumin is restricted across the GBM by what
|
charge
|
|
|
60 - 80 Kd size of what
|
albumin
|
|
|
the major cause of proteinuria
|
Permeability of GBM is altered allowing increased filtration
of normal plasma proteins this is called glomerular proteinuria |
|
|
Filtration of a plasma protein present in large amounts is called
|
overflow proteinuria
|
|
|
what disease causes overflow proteinuris which is Filtration of a plasma protein present in large amounts
|
Multiple myeloma
|
|
|
– Causes massive proteinuria and renal failure
– No extrarenal manifestations – ESRD by age 2 – Transplantation curative |
• Congenital nephrotic syndrome of the Finnish type
– Mutation in the gene encoding nephrin |
|
|
what is nephrin
|
slit diaphragm protein
|
|
|
• Dipstick detects primarily
|
albumin
|
|
|
Normal albumin excretion
|
30 mg/day
|
|
|
Dipstick detects primarily albumin
– Becomes positive at |
• Dipstick detects primarily albumin
– Normal albumin excretion < 30 mg/day – Becomes positive at >300 mg/day |
|
|
Dipstick is Insensitive to
|
– Low levels of albumin excretion (30-300)
microalbuminuria) – Does not detect other proteins (immunoglobulin light chains) |
|
|
urine gold standard for proteinuria
|
24 hour urine gold standard (normal < 150
mg/day) or Urine protein/creatinine ratio (normal < 0.5 mg/mg age 6 months‐2 years, normal < 0.2 mg/mg age 2 years on) |
|
|
Urine protein/creatinine ratio normal is what?
|
(normal < 0.5
mg/mg age 6 months‐2 years, normal < 0.2 mg/mg age 2 years on |
|
|
Albumin/creatinine ratio
|
(normal < 30 mg/g)
|
|
|
Diabetic nephropathy is the most common cause
|
• Glomerular disease
– Diabetic nephropathy is the most common cause of proteinuria and end end‐stage renal disease |
|
|
– Intraglomerular inflammation
– Cellular proliferation – Hematuria – Excludes nonproliferative disorders |
• Definition of glomerulonephritis (GN)
|
|
|
• Definition of glomerulonephritis (GN)
|
– Intraglomerular inflammation
– Cellular proliferation – Hematuria – Excludes nonproliferative disorders |
|
|
• Proteinuria
– > 3.5 g/day/1.73 m 2 adult – > 40 mg/hr/m 2 child • Hypoalbuminemia < 3.5 g/dL • Edema (generalized – anasarca) • Hyperlipidemia • Lipiduria |
Nephrotic Syndrome
|
|
|
Nephrotic Syndrome
|
• Proteinuria
– > 3.5 g/day/1.73 m 2 adult – > 40 mg/hr/m 2 child • Hypoalbuminemia < 3.5 g/dL • Edema (generalized – anasarca) • Hyperlipidemia • Lipiduria |
|
|
albumin in nephrotic
|
• Hypoalbuminemia < 3.5 g/dL
|
|
|
– Hypercoagulability (deep venous thrombosis,
pulmonary embolus, renal vein thrombosis) – Vitamin D deficiency (osteomalacia) – Increased risk of infection – Hypertension – Increased cardiovascular morbidity – Hypovolemia and acute renal failure |
Nephrotic Syndrome
• Complications |
|
|
Nephrotic Syndrome
• Complications |
– Hypercoagulability (deep venous thrombosis,
pulmonary embolus, renal vein thrombosis) – Vitamin D deficiency (osteomalacia) – Increased risk of infection – Hypertension – Increased cardiovascular morbidity – Hypovolemia and acute renal failure |
|
|
why specifically is someone at risk to become hypercoagulable in nephrotic syndrome
|
loss of AT 3 in the urine
|
|
|
loss of AT 3 in the urine
|
why specifically is someone at risk to become hypercoagulable in nephrotic syndrome
|
|
|
What nephrotic syndrome most often manifests the hypercoag
|
membranous types of nephropathy
|
|
|
bone disease seen in nephrotic syndrome
|
osteomalacia
|
|
|
why do people with nephrotic disease become Hypertensive?
|
their underlying glomerular disease leads to salt and water retention.
this leads to increased risk to cardiovascular disease. |
|
|
• Treatment
– ACE (angiotensin converting enzyme) inhibitors, ARB’s (angiotensin receptor blockers) • Evidence from randomized controlled trials in diabetic nephropathy have shown benefit Protein restriction – 0.6g/kg/day (guidelines) – Diabetes control – target A1C < 7 – Sodium restriction and diuretic therapy for edema |
diabetic nephropathy Tx
|
|
|
diabetic nephropathy Tx
|
• Treatment
– ACE (angiotensin converting enzyme) inhibitors, ARB’s (angiotensin receptor blockers) • Evidence from randomized controlled trials in diabetic nephropathy have shown benefit Protein restriction – 0.6g/kg/day (guidelines) – Diabetes control – target A1C < 7 – Sodium restriction and diuretic therapy for edema |
|
|
• Too many cellsÞclosure of capillary loops
|
Glomerulonephritis
(Nephritic Syndrome) |
|
|
Glomerulonephritis
(Nephritic Syndrome) is characterized by |
Glomerulonephritis
(Nephritic Syndrome) • Characterized by inflammation and proliferation of the glomeruli • Too many cellsÞclosure of capillary loops • Immune mediated (majority) • Clinical presentation varies – Asymptomatic hematuria – Acute nephritis – Rapidly progressive GN |
|
|
• Immune mediated (majority
|
Glomerulonephritis
(Nephritic Syndrome) • Characterized by inflammation and proliferation of the glomeruli • Too many cellsÞclosure of capillary loops • Immune mediated (majority) • Clinical presentation varies – Asymptomatic hematuria – Acute nephritis – Rapidly progressive GN |
|
|
• Characterized by inflammation and proliferation of
the glomeruli |
Glomerulonephritis
(Nephritic Syndrome) • Characterized by inflammation and proliferation of the glomeruli • Too many cellsÞclosure of capillary loops • Immune mediated (majority) • Clinical presentation varies – Asymptomatic hematuria – Acute nephritis – Rapidly progressive GN |
|
|
• Hematuria – dysmorphic red blood cells, red
blood cell casts • Azotemia (elevated BUN and Cr) • Oliguria (decreased urine output) |
(Nephritic Syndrome)
|
|
|
(Nephritic Syndrome) has what manifestations
|
• Hematuria – dysmorphic red blood cells, red
blood cell casts • Azotemia (elevated BUN and Cr) • Oliguria (decreased urine output) • Hypertension • Variable proteinuria |
|
|
casts of nephrotic syndrome
|
fatty hyaline
|
|
|
casts of nephritic syndrome
|
rbc
|
|
|
cells of the urine in nephrotic
|
rare
|
|
|
cells in the urine of nephritic
|
RBCs that are dysmorphic
|
|
|
dysmorphic RBCs seen in what nephritic or nephrotic
|
nephritic
|
|
|
describe the MOA of glomerular injury
|
Mechanisms of Injury
• Initial insult • Nephron loss • Nephron hypertrophy • Afferent arteriolar vasodilatation • Increase glomerular capillary pressure • Alteration in GBM Þ proteinuria |
|
|
Causes of primary idiopathic NS
|
– Minimal change disease
– Membranous nephropathy – Focal segmental glomerulosclerosis – Membranoproliferative GN (overlap) |
|
|
– Minimal change disease
– Membranous nephropathy – Focal segmental glomerulosclerosis – Membranoproliferative GN (overlap) |
Causes of primary idiopathic NS
|
|
|
can be both nephritic nephrotic
|
Membranoproliferative GN
|
|
|
• Causes of secondary NS
|
– Minimal change disease
– Membranous nephropathy – Focal segmental glomerulosclerosis – Membranoproliferative GN – Diabetic nephropathy (unique pathology) – Amyloid (unique pathology) – Light change deposition disease (unique pathology |
|
|
– Minimal change disease
– Membranous nephropathy – Focal segmental glomerulosclerosis – Membranoproliferative GN – Diabetic nephropathy (unique pathology) – Amyloid (unique pathology) – Light change deposition disease (unique pathology |
– Minimal change disease
– Membranous nephropathy – Focal segmental glomerulosclerosis – Membranoproliferative GN – Diabetic nephropathy (unique pathology) – Amyloid (unique pathology) – Light change deposition disease (unique pathology |
|
|
Minimal Change Disease secondary causes
|
• Secondary causes
– Nonsteroidal anti‐inflammatory agents – Malignancies (lymphoproliferative disease, e.g. Hodgkin’s lymphoma) Minimal Change Disease • Most cases occur in children • Most cases primary or idiopathic • Secondary causes – Nonsteroidal anti‐inflammatory agents – Malignancies (lymphoproliferative disease, e.g. Hodgkin’s lymphoma) • Steroid responsive (prednisone) |
|
|
– Nonsteroidal anti‐inflammatory agents
– Malignancies (lymphoproliferative disease, e.g. Hodgkin’s lymphoma) |
• Secondary causes of MCD
– Nonsteroidal anti‐inflammatory agents – Malignancies (lymphoproliferative disease, e.g. Hodgkin’s lymphoma) |
|
|
• More common in adults
• More common in African Americans • Usually primary or idiopathic |
Focal Segmental Glomerulosclerosis
|
|
|
Focal Segmental Glomerulosclerosis
• Secondary causes |
Focal Segmental Glomerulosclerosis
• Secondary causes – Healing of previous glomerular injury – Morbid obesity – ? Obstructive sleep apnea – Sickle cell anemia – HIV – Heroin abuse – Vesicoureteral reflux – Medications (pamidronate) |
|
|
HIV for what
|
collapsing FSGS
|
|
|
(pamidronate
|
causes FSGS
|
|
|
• Most common cause of primary nephrotic
syndrome in adults • 5 th and 6 th decades |
Membranous Nephropathy
• Most common cause of primary nephrotic syndrome in adults • 5 th and 6 th decades • More common in Caucasians • Immune complex disease • Higher incidence of renal vein thrombosis • Slowly progressive disorder with variable response to immunosuppressant agents |
|
|
• Higher incidence of renal vein thrombosis
|
Membranous Nephropathy
• Most common cause of primary nephrotic syndrome in adults • 5 th and 6 th decades • More common in Caucasians • Immune complex disease • Higher incidence of renal vein thrombosis • Slowly progressive disorder with variable response to immunosuppressant agents |
|
|
• Slowly progressive disorder with variable
response to immunosuppressant agents |
Membranous Nephropathy
|
|
|
Membranous Nephropathy
• Secondary causes |
Membranous Nephropathy
• Secondary causes – Malignancy, primarily solid tumors – SLE class V – Rheumatoid arthritis – Hepatitis B and C – Drugs (penicillamine, gold, captopril) – Syphilis |
|
|
– SLE class V
|
Membranous Nephropathy
• Secondary causes – Malignancy, primarily solid tumors – SLE class V – Rheumatoid arthritis – Hepatitis B and C – Drugs (penicillamine, gold, captopril) – Syphilis |
|
|
– Drugs (penicillamine, gold, captopril)
|
Membranous Nephropathy
• Secondary causes – Malignancy, primarily solid tumors – SLE class V – Rheumatoid arthritis – Hepatitis B and C – Drugs (penicillamine, gold, captopril) – Syphilis |
|
|
– Syphilis
|
Membranous Nephropathy
• Secondary causes – Malignancy, primarily solid tumors – SLE class V – Rheumatoid arthritis – Hepatitis B and C – Drugs (penicillamine, gold, captopril) – Syphilis |
|
|
Rheumatoid arthritis
|
Membranous Nephropathy
• Secondary causes – Malignancy, primarily solid tumors – SLE class V – Rheumatoid arthritis – Hepatitis B and C – Drugs (penicillamine, gold, captopril) – Syphilis |
|
|
– Active urine sediment
– No or minimal renal failure – Low grade proteinuria |
• Focal glomerulonephritis
|
|
|
calssification of Focal Glomerulonephritis
|
• Focal glomerulonephritis
– Active urine sediment – No or minimal renal failure – Low grade proteinuria |
|
|
– No or minimal renal failure
|
• Focal glomerulonephritis
– Active urine sediment – No or minimal renal failure – Low grade proteinuria |
|
|
• Diffuse glomerulonephritis
|
Diffuse glomerulonephritis
– Active urine sediment – Renal failure – Variable proteinuria, can be nephrotic |
|
|
– IgA nephropathy
– SLE class II and III – Henoch‐Schonlein purpura – Heriditary nephritis (Alport syndrome) |
• Focal glomerulonephritis
|
|
|
causes of
|
– IgA nephropathy
– SLE class II and III – Henoch‐Schonlein purpura – Heriditary nephritis (Alport |
|
|
– SLE class II and III
|
• Focal glomerulonephritis
• Focal glomerulonephritis – IgA nephropathy – SLE class II and III – Henoch‐Schonlein purpura – Heriditary nephritis (Alport syndrome) |
|
|
– Henoch‐Schonlein purpura
|
• Focal glomerulonephritis
• Focal glomerulonephritis – IgA nephropathy – SLE class II and III – Henoch‐Schonlein purpura – Heriditary nephritis (Alport syndrome) |
|
|
– IgA nephropathy
|
• Focal glomerulonephritis
– IgA nephropathy – SLE class II and III – Henoch‐Schonlein purpura – Heriditary nephritis (Alport syndrome) |
|
|
– SLE class IV
|
• Diffuse glomerulonephritis
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
• Diffuse glomerulonephritis causes
|
• Diffuse glomerulonephritis causes
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
• Goodpasture’s syndrome
|
• Diffuse glomerulonephritis causes
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
– SLE class IV
|
• Diffuse glomerulonephritis
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
– Membranoproliferative GN
|
• Diffuse glomerulonephritis causes
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
– Bacterial endocarditis
– Membranoproliferative GN |
• Diffuse glomerulonephritis causes
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
• ANCA associated GN
|
• Diffuse glomerulonephritis causes
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
– Membranoproliferative GN
|
• Diffuse glomerulonephritis
– Poststreptococcal GN – Bacterial endocarditis – Membranoproliferative GN – SLE class IV – Rapidly progressive GN • Goodpasture’s syndrome • ANCA associated GN |
|
|
Most common form of primary GN worldwide
|
IgA
|
|
|
– Age 20‐30
– Males > Females |
IgA Nephropathy
– Most common form of primary GN worldwide – Immune complex mediated GN – Asians and Caucasians – Rare in African‐Americans – Age 20‐30 – Males > Females – Pathogenesis – altered regulation of IgA |
|
|
IgA Nephropathy
• Clinical presentation |
• Clinical presentation
– 50‐60% episodic gross hematuria (synpharyngitic) – 30% persistent microscopic hematuria – 10% acute glomerulonephritis – ESRD 20‐40% at 5‐25 years |
|
|
IgA deposits are where
|
mesangial
|
|
|
complement levels in IgA nephropathy
|
normal
|
|
|
(synpharyngitic)
|
IgA Nephropathy
– Most common form of primary GN worldwide – Immune complex mediated GN – Asians and Caucasians – Rare in African‐Americans – Age 20‐30 – Males > Females – Pathogenesis – altered regulation of IgA |
|
|
• Peak age 4‐5 years
• Acute onset, self‐limited • Gross hematuria not common • Renal abnormalities usually resolve |
Henoch‐Schonlein Purpura
|
|
|
complement levels of Poststreptococcal Glomerulonephritis
|
Poststreptococcal Glomerulonephritis
• Clinical presentation – Children 2‐10 years – Uncommon over age 40 (< 10%) – Symptoms develop 2 weeks after throat infection, longer for skin infections – Low complement levels (C 3 – Spontaneous recovery is the rule – Hematuria can persist 6 months – Proteinuria, mild can persist years and CH50) |
|
|
Poststreptococcal Glomerulonephritis
• Pathogenesis – Nephritogenic strains of group A streptococci |
Poststreptococcal Glomerulonephritis
• Pathogenesis – Nephritogenic strains of group A streptococci ( hemolytic Streptococcus • Zymogen • Nephritis plasmin‐binding protein – Host immune response (ab/ag) – Trapping of immune complexes – IgG and C 3 found in glomeruli β Streptococcus), type 12 |
|
|
Rapidly Progressive Glomerulonephritis
• Immune complex mediated: |
Rapidly Progressive Glomerulonephritis
• Immune complex mediated: – IgA nephropathy – Cryoglobulinemia – Lupus nephritis – Acute postinfectious GN – Membranoproliferative GN |
|
|
Rapidly Progressive Glomerulonephritis
?????? mediated: – IgA nephropathy – Cryoglobulinemia – Lupus nephritis – Acute postinfectious GN – Membranoproliferative GN |
Rapidly Progressive Glomerulonephritis
• Immune complex mediated: – IgA nephropathy – Cryoglobulinemia – Lupus nephritis – Acute postinfectious GN – Membranoproliferative GN |
|
|
– Bimodal age distribution
|
Anti‐GBM Disease and
Goodpasture Syndrome • Clinical presentation: – Bimodal age distribution (3 – 60‐70% present with pulmonary hemorrhage Goodpasture Syndrome (smokers) – Systemic symptoms ‐ malaise, fatigue, anorexia, weight loss, arthralgias, myalgias – Male Caucasians – Rare in African‐Americans |
|
|
Anti‐GBM Disease and
Goodpasture Syndrome • Pathogenesis – Antibodies develop against |
Anti‐GBM Disease and
Goodpasture Syndrome • Pathogenesis – Antibodies develop against collagen in GBM – Predisposing factors include both genetic and environmental – Linear deposition of IgG along GBM – Antibodies detected by ELISA 90% of cases – ANCA found in 15‐30% of patients a3 chain type IV |
|
|
– Corticosteroids alone insufficient
– Cyclophosphamide – Plasma exchange with albumin 14 days |
Anti‐GBM Disease and
Goodpasture Syndrome • Pathogenesis – Antibodies develop against collagen in GBM – Predisposing factors include both genetic and environmental – Linear deposition of IgG along GBM – Antibodies detected by ELISA 90% of cases – ANCA found in 15‐30% of patients a3 chain type IV |
|
|
– Corticosteroids alone insufficient
– Cyclophosphamide – Plasma exchange with albumin 14 days |
Anti‐GBM Disease and
Goodpasture Syndrome • Outcome poor without therapy • Treatment – Corticosteroids alone insufficient – Cyclophosphamide – Plasma exchange with albumin 14 days • Renal recovery rare if patients present needing dialysis (Cr > 6 mg/dL) |
|
|
– Plasma exchange with albumin 14 days
|
Anti‐GBM Disease and
Goodpasture Syndrome • Outcome poor without therapy • Treatment – Corticosteroids alone insufficient – Cyclophosphamide – Plasma exchange with albumin 14 days • Renal recovery rare if patients present needing dialysis (Cr > 6 mg/dL) |
|
|
• Class I –sle neph
|
Classification of Lupus Nephritis
• Class I – minimal changes, < 5% biopsies • Class II – mesangial disease, 10 • Class III – focal proliferative GN, 20 • Class IV – diffuse proliferative GN, 35 • Class V – membranous nephropathy, 10 biopsies • Class VI – chronic sclerosing nephropathy 10‐25% biopsies 20‐35% biopsies 35‐60% biopsies 10‐15% |
|
|
• Class II
|
Classification of Lupus Nephritis
• Class I – minimal changes, < 5% biopsies • Class II – mesangial disease, 10 • Class III – focal proliferative GN, 20 • Class IV – diffuse proliferative GN, 35 • Class V – membranous nephropathy, 10 biopsies • Class VI – chronic sclerosing nephropathy 10‐25% biopsies 20‐35% biopsies 35‐60% biopsies 10‐15% |
|
|
• Class III
|
Classification of Lupus Nephritis
• Class I – minimal changes, < 5% biopsies • Class II – mesangial disease, 10 • Class III – focal proliferative GN, 20 • Class IV – diffuse proliferative GN, 35 • Class V – membranous nephropathy, 10 biopsies • Class VI – chronic sclerosing nephropathy 10‐25% biopsies 20‐35% biopsies 35‐60% biopsies 10‐15% |
|
|
• Class III
|
Classification of Lupus Nephritis
• Class I – minimal changes, < 5% biopsies • Class II – mesangial disease, 10 • Class III – focal proliferative GN, 20 • Class IV – diffuse proliferative GN, 35 • Class V – membranous nephropathy, 10 biopsies • Class VI – chronic sclerosing nephropathy 10‐25% biopsies 20‐35% biopsies 35‐60% biopsies 10‐15% |
|
|
• Class IV
|
Classification of Lupus Nephritis
• Class I – minimal changes, < 5% biopsies • Class II – mesangial disease, 10 • Class III – focal proliferative GN, 20 • Class IV – diffuse proliferative GN, 35 • Class V – membranous nephropathy, 10 biopsies • Class VI – chronic sclerosing nephropathy 10‐25% biopsies 20‐35% biopsies 35‐60% biopsies 10‐15% |
|
|
• Class V
|
Classification of Lupus Nephritis
• Class I – minimal changes, < 5% biopsies • Class II – mesangial disease, 10 • Class III – focal proliferative GN, 20 • Class IV – diffuse proliferative GN, 35 • Class V – membranous nephropathy, 10 biopsies • Class VI – chronic sclerosing nephropathy 10‐25% biopsies 20‐35% biopsies 35‐60% biopsies 10‐15% |
|
|
– Corticosteroids
– Azathioprine – Cyclophosphamide – Mycophenolate mofetil |
Lupus Nephritis
• Treatment – Corticosteroids – Azathioprine – Cyclophosphamide – Mycophenolate mofetil |
|
|
– Azathioprine
|
Lupus Nephritis
• Treatment – Corticosteroids – Azathioprine – Cyclophosphamide – Mycophenolate mofetil |
|
|
– Mycophenolate mofetil
|
Lupus Nephritis
• Treatment – Corticosteroids – Azathioprine – Cyclophosphamide – Mycophenolate mofetil |
|
|
• Low serum complement level
– Systemic diseases |
• Low serum complement level
– Systemic diseases • SLE (75‐90%) • Subacute bacterial endocarditis (90%) • Cryoglobulinemia (85%) |
|
|
– Systemic diseases
• SLE (75‐90%) • Subacute bacterial endocarditis (90%) • Cryoglobulinemia (85%) |
• Low serum complement level
– Systemic diseases • SLE (75‐90%) • Subacute bacterial endocarditis (90%) • Cryoglobulinemia (85%) |
|
|
• Acute poststreptococcal glomerulonephritis (90%)
• Membranoproliferative glomerulonephritis (90%) |
Laboratory Tests
• Low serum complement level – Systemic diseases • SLE (75‐90%) • Subacute bacterial endocarditis (90%) • Cryoglobulinemia (85%) – Renal diseases • Acute poststreptococcal glomerulonephritis (90%) • Membranoproliferative glomerulonephritis (90%) ‐ Complements |
|
|
• Normal serum complement level
– Systemic diseases |
• Normal serum complement level
– Systemic diseases • Vasculitis • Henoch‐Schonlein purpura |
|
|
• Normal serum complement level
– Renal diseases |
• IgA nephropathy
• Rapidly progressive glomerulonephritis – ANCA associated GN – Anti‐GBM disease |
