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GNs and AKI Flashcards

1
Q

List the different ways HIV can cause kidney disease

A
  1. Glomerular disease
    1. HIV-associated nephropathy (collapsing FSGS)
    2. HIV immune complex kidney disease
    3. HIV-associated TMA
    4. Rare:
      1. MPGN+/- cryoblogulin-associated vasculitis
      2. Membranous
      3. Fibrillary, imunotactoid
      4. Amyloid
      5. Minimal change
  2. Tubular (med-related)
    1. AKI (aminoglycosides, cidofovir)
    2. Proximal tubule (Fanconi) - tenofovir, etc.
    3. DI - tenofovir, amphotericin, etc.
    4. Chronic tubular injury
    5. Crystal nephropathy - indinavir
  3. Interstitial - meds
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2
Q

Pathology for membranous nephropathy

A
  • LM: GBM spikes, GBM thickening
  • IF: Diffuse granular IgG and C3 along GBM
  • EM: Foot process effacement, subepithelial electron-dense deposits
    • Ehrenreich-Churg EM Classification (no clinical or prognostic significance):
      • Stage I: deposits without basement membrane reaction
      • Stage II: basement membrane spikes between deposits
      • Stage III: basement membrane material between and surrounding deposits
      • Stage IV: electron lucent areas consistent with resportion of subepithelial immune complexes
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3
Q

Causes of secondary membranous nephropathy?

A
  1. Autoimmune: SLE, (RA, IgG-4, autoimmune thyroid dz, anti-GBM and ANCA GN)
  2. Infection: HepB, (HCV, HIV, syphilis, schistosomiasis)
  3. Malignancy: Solid tumors e.g colon, stomach, lung, prostate, (NHL, CLL, melanoma)
  4. Drugs/toxins: NSAIDs and COX-2 inhibitors, (gold, penicillamine, mercury)
  5. Miscellaneous: Sarcoidosis, anticationic bovine serum albumin
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4
Q

Drug causes of membranous nephropathy

A

penicillamine, gold, NSAIDs, mercury, captopril (high dose), TNF-inhibitors (infliximab, adalimumab, etanercept)

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5
Q

Indications to treat membranous nephropathy?

A
  1. At the time of diagnosis, high risk for progression if >=2 of:
    1. Cr >=133
    2. Progressive decline in GFR >=25% from baseline over last 2 years
    3. Severe nephrotic syndrome, defined as any of:
      1. Albumin <25- (bromocresol green) or <20 (bromocresol purple)
      2. Refractory edema
      3. VTE
  2. Persistent/worsening nephrotic proteinuria/GFR/anti-PLA2R levels despite 3-6 months supportive tx and observation
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6
Q

Management of primary membranous nephropathy?

A
  1. Conservative
    1. Edema: low Na diet, diuretic
    2. Proteinuria: ACE/ARB
    3. Hyperlipidemia: statin (LDL <2)
    4. Anticoagulation: consider if albumin <20-25, heavy proteinuria esp >10g/d
  2. Immunosuppressive therapy
    1. Ponticelli - Steroids (months 1, 3, 5) + CYC (months 2, 4, 6)
    2. Rituximab
    3. Calcineurin inhibitors
    4. ACTH
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7
Q

Cholesterol emboli: 3 risk factors, 3 procedures, and 3-4 clinical/non-renal manifestations?

A
  • Risk factors for cholesterol emboli
  • In the setting of vascular manipulation of the aorta
    • 1)Male
    • 2)Age >50
    • 3)Risk factors for atherosclerosis: smoking, hypercholesterolemia, obesity, diabetes
  • Procedures that may increase risk of cholesterol emboli
    • 1)Angiography
    • 2)AAA repair
    • 3)CABG
    • 4)Valve replacement (especially TAVI)
    • 5)Intra-aortic balloon pump
  • Manifestations of cholesterol emboli
    • Renal
      • 1)Subacute renal impairment within 1-2 weeks of inciting event (progressing over weeks to months)
      • 2)Stuttering course
      • 3)Little or no recovery of renal function
      • 4)Bland urinalysis
    • Non-renal
    • 1)Timing 1-2 weeks after vascular manipulation
    • 2)Eosinophilia
    • 3)Hypocomplementemia
    • 4)Signs of extrarenal atheroemboli (cyanosis, discrete gangrenous lesions, livedo reticularis, TIA/amarosis fugax/hollenhorst plaques, mesenteric ischemia)
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8
Q

Patient-related risk factors and procedure-related risk factors for AKI after cardiac surgery?

A
  • Patient
    • 1.Age
    • 2.CHF
    • 3.Preoperative IABP/Cardiogenic Shock
    • 4.Diabetes
    • 5.Pre-operative CKD
    • 6.Chronic Lung Disease
  • B) Procedure
    • 1.Length of cardiopulmonary bypass
    • 2.Duration of aortic cross-clamping
    • 3.Off-pump vs on-pump CABG
    • 4.CABG only vs. Valve only vs. CABG + Valve
    • 5.Reoperation
  • (Based on Clevland and Mehta scores)
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9
Q

What is an MPGN histologic pattern?

A
  • Pathologic pattern of subendothelial and mesangial deposition of immune complexes and/or complement factors with proliferative changes in the glomeruli
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10
Q

Categories and causes of MPGN?

A
  • Immune-complex mediated
    • Infection:
      • Viral: HCV and HBV (cryoglobulinemic GN), HIV
      • Bacterial: endocarditis, infected ventriculoatrial shunt, visceral abscesses, leprosy, meningococcal meningitis
      • Protozoa/other: malaria, schistosomiasis, mycoplasma, leishmaniasis
    • Autoimmune: SLE, RA, Sjogren’s, undifferentiated CTD, PSC, Grave’s
    • Malignancy: MM, lymphoma, Waldenstrom macroglobulinemia, MGRS
    • Fibrillary GN
  • Complement-mediated
    • DDD
    • C3GN
    • GN with dominant C3
  • MPGN without immune-complex or complement
  • “Idiopathic”
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11
Q

Difference between the C3 glomerulopathies?

A
  • Dense deposit disease: a form of C3G with characteristic EM appearance of intensely osmiophilic transformation of GBM
  • C3 glomerulonephritis: C3 glomerulopathy without the characteristic appearances of DDD
  • Glomerulonephritis with dominant C3: morphologic term for cases of GN with dominant staining for C3c (>=2 orders of magnitude than other immune reactant). Many will represent C3G.
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12
Q

Pathophysiology of C3 glomerulopathy?

A
  • Problem with the alternative complement pathway/excess activation
  • Normally, the alternative complement pathway is always activated but at a very low rate -> constant generation of small accounts of activated C3
  • When there’s a pathogen, there is rapid amplification of C3b (positive C3b amplification loop) -> millions of C3b molecules within minutes.
  • Therefore, systems are in place to prevent inappropriate activation of the pathway:
    • C factor H (CFH): inhibits C3b amplification (by binding to C3b
  • Factor H-related proteins (CHFR): promotes C3b amplification, by inhibiting CFH
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13
Q

Caues of C3 glomerulopathy?

A
  • Genetic
    • Complement-regulating proteins: CFH, CFI, CFHR5
    • Antibodies to complement regulating proteins: C3Nef, Ab against CFH, CFI, or CFB
    • Complement factors: C3, CFB
  • Infection
  • Paraproteinemia
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14
Q

Pathology findings (LM, IF, EM) for C3GN

A
  • LM: variable.
    • MPGN pattern (glomerular lobulation, increased mesangial matrix/cells, capillary wall thickening with double contouring)
    • PIGN pattern (diffuse endocapillary proliferative GN)
  • IF: Granular C3 staining in capillary walls and mesangium. C3 at least 2 orders of magnitude compared with others.
  • EM:
    • DDD: Osmiophilic dense transformation of GBM, large densities in the mesangium
    • C3GN: electron-dense material expands the GBM but without marked density as in DDD
    • Both: subepithelial humps/deposits (like PIGN)
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15
Q

What is ocular drusen and which GN can you see this?

A

Lipoprotein deposits of complement-containing debris in retinal epithelium

Seen in DDD

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16
Q

Patient and procedure-related risk factors for choelsterol emboli syndrome?

A
  • Patient:
    • Male
    • Age >50
    • Risk factors for atherosclerosis: smoking, hypercholesterolemia, obesity, diabetes
  • Procedure:
    • Angiography
    • AAA repair
    • CABG
    • Valve replacement (especially TAVI)
    • Intra-aortic balloon pump
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17
Q

Renal manifestations of cholesterol emboli syndrome

A
  • Renal
    1. Subacute renal impairment within 1-2 weeks of inciting event (progressing over weeks to months)
    2. Stuttering course
    3. Little or no recovery of renal function
    4. Bland urinalysis
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18
Q

Non-renal manifestations of cholesterol emboli syndrome

A
  1. Timing 1-2 weeks after vascular manipulation
  2. Eosinophilia
  3. Hypocomplementemia
  4. Signs of extrarenal atheroemboli (cyanosis, discrete gangrenous lesions, livedo reticularis, TIA/amarosis fugax/hollenhorst plaques, mesenteric ischemia)
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19
Q

Overall management of ligh chain cast nephropathy?

A
  • Anti-myeloma therapy (CyBorD)
  • Stop all nephrotoxins
  • Correct hypercalcemia
  • Fluids, target urine output 3L/day
  • Urinary alkalinization
  • Avoid loop diuretocs
  • Dialysis
  • +/- High-cutoff dialysis, plasmapheresis
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20
Q

Reasons for diuretic resistance?

A
  1. Poor GFR with inappropriately low dose
  2. Fluid and salt dietary non-compliance
  3. Low albumin
  4. Anasarca with poor gut absorption
  5. Rebound Na uptake after volume loss
  6. RAS activation
  7. Hypertrophy of distal nephron
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21
Q

5 types of cardiorenal syndrome

A
  • Type 1 (acute) – Acute HF results in acute kidney injury
  • Type 2 – Chronic cardiac dysfunction (eg, chronic HF) causes progressive chronic kidney disease
  • Type 3 – Abrupt and primary worsening of kidney function due, for example, to renal ischemia or glomerulonephritis causes acute cardiac dysfunction, which may be manifested by HF.
  • Type 4 – Primary CKD contributes to cardiac dysfunction, which may be manifested by coronary disease, HF, or arrhythmia.
  • Type 5 (secondary) – Acute or chronic systemic disorders (eg, sepsis or diabetes mellitus) that cause both cardiac and renal dysfunction.
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22
Q

Causes of renal failure in Crohn’s disease

A
  • IgAN
  • Kidney stones/obstruction
  • AIN secondary to meds (5-ASA, NSAIDs)
  • MCD secondary to 5-ASA, NSAIDs
  • Drug-induced SLE (anti-TNF)
  • Membranous, secondary (anti-TNF)
  • Secondary amyloidosis (AA)
  • Prerenal from diarrhea
  • ATN from intra-abdo sepsis
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23
Q

Renal manifestations of sickle cell disease

A
  1. Sickle cell nephropathy
  2. Renal infarction, papillary necrosis
  3. UTI, pyelonephritis
  4. Renal medullary carcinoma
  5. BP abnormalities (hypo or hypertension)
  6. Hyperuricemia, gout
  7. Hyperkalemia
  8. Enuresis
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24
Q

Worst renal disease from sickle cell trait?

How to diagnose?

A

Renal medullary carcinoma - rare, aggressive cancer

CT or MRI (US not sensitive enough) +/- scans to look for metastatic disease

Prognosis poor

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25
Q

HIVAN clinical presentation?

A
  • African American ethnicity
  • Advanced HIV disease – high viral load, low CD4 count
  • Heavy proteinuria
  • Rapid decline in kidney function
  • Other – hematuria, HTN, edema
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26
Q

Treatment of HRS

A
  • Albumin 1mg/kg (to max 100g divided twice per day), Midodrine 7.5-15mg PO TID, Octreotide 100-200mg TID
  • Liver transplant
  • NE or Terlipressin
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27
Q

Diagnosis of HRS

A
  • Cirrhosis + ascites
  • AKI
  • NO response after diuretic withdrawal for 2 days and volume expansion with albumin (1g/kg body wt)
  • Absence of shock
  • No concurrent nephrotoxic drugs
  • No structural kidney disease (normal US, no proteinuria or hematuria)
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28
Q

Differentiation of type 1 and 2 HRS

A
  • Type 1: double of creatnine in 2 weeks or less
  • Type 1: higher mortality
  • Type 2: major feature is diuretic resistant ascites
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29
Q

Absolute and Relative contraindications to kidney biopsy

A
  • Uncontrolled BP
  • Bleeding diathesis
  • Uncooperative patient/no consent
  • Infection over biopsy site
  • Small, hyperechoic kidneys (less than 9cm)
  • Solitary native kidney
  • Hydronephrosis
  • Renal or peri-renal infection
  • Multiple, bilateral cysts
  • Pregnancy?
  • Uncooperative patient
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30
Q

How to diagnose orthostatic proteinuria?

A
  • 24-hr split urine collection
    • Discard first AM void
    • Collect all day until bed, lie down 2 hrs before bed -> orthostatic collection
    • Collect all night and AM firstvoid -> recumbent collection
  • Orthostatic proteinuria is diagnosed if the urinary protein excretion rate is normal for the nighttime collection (adults <50 mg over an eight-hour period) and the daytime collection exceeds the normal protein excretion rate.
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31
Q

Causes of CKD in oncology

A
  • Use of nephrotoxic chemo
  • Age at diagnosis
  • Chronic pre-renal disease
  • Pre-existing comorbid conditions, HTN, DM
  • Pre-renal – diarrhea, poor oral intake
  • ATN – chemotherapy, N/V/dehydration
  • TLS – with therapy
  • Obstruction – based on extent of malignancy
  • Radiation nephritis
  • GN from malignancy
  • Hypercalcemia
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32
Q

Minimal change disease definitions: complete vs. partial remission, steroid-senitive, -resistant, -dependent, frequently relapsing

A
  • Remission:
    • Resolution of edema
    • Normalization of albumin >=35
    • Marked reduction in proteinuria
  • “Complete” remission – Proteinuria <0.3 g/day
  • “Partial” remission – Proteinuria <3.5 g/day AND decrease >50%
  • Steroid-sensitive – response with pred 1mg/kg/d within 16wks
  • Steroid-resistant – no response with pred 1mg/kg/d within 16 wks
  • Steroid-dependent – relapse during therapy or within 15 days of stoping
  • Infrequently-relapsing - <2 relapse/6 months (<4 relapse/12 months)
  • Frequently-relapsing - >=2 relapse/6 months (>=4 relapse/12 months)
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33
Q

MCD secondary causes

A
  • Drugs: NSAIDs, lithium (usually chronic interstitial nephritis), gold (usually membranous), interferon-alpha, tyrosine kinase inhibitors
  • Allergy: Pollens, house dust, bee sting, immunizations, poison oak
  • Autoimmune: SLE, celiac, myasthenia gravis, autoimmune pancreatitis, diabetes, allogenic stem cell transplant
  • Infections: Mycoplasma pneumoniae, viral, parasitic
  • Malignancy: Hodgkin disease, NHL, CLL (usually MPGN), MM, mycosis fungoides
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34
Q

Pathogenesis of MCD

A

Possibly impaired T cell regulation and circulating factors that permits permeability and foot process effacement

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35
Q

4 mechanisms for increased edema in nephrotic syndrome?

A
  1. Lack of oncotic pressure
  2. Sodium retention (w/ increased ENaC activity)
  3. Fluid retention
  4. AKI
  5. Increased capillary permeability in the peripheral capillary beds
  6. Dietary Na non-adherance
  7. Diuretic resistance
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36
Q

4 mechanisms for VTE in nephrotic syndrome

A
  1. Urinary losses of:
    1. anti-thrombin III
    2. plasminogen
    3. Protein C
    4. Protein S
  2. Increased platelet activation
  3. Hyperfibrinogenemia
  4. Venous stasis due to edema
  5. Hemoconcentration in renal vein – hemoconcentration post glomerular + diuretics
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37
Q

Pathology of MCD

A
  • LM: Normal.
  • IF: Negative. +/- mesangial IgA, C1q.
  • EM: Diffuse FPE. Normal GBM. No deposits
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38
Q

Medical treatment options for MCD

A
  • Prednisone 1mg/kg/d x 4-16 wks, taper over6 months
    • Late relapse (>4 wks), do same
    • Early relapse (<4 wks), longer taper
  • Cyclophosphamide 2mg/kg/day x 12 weeks
  • CNI (Cyclosporine or Tacrolimus)
  • Rituximab
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39
Q

Side effects of non-steroid treatments for MCD?

A
  • Cyclophosphamide – infertility, hemorrhagic cystitis, increased malignancy, cytopenias, teratogenicity, alopecia
  • CNI – Hypertension, Diabetes, AKI, CKD, TMA, Gingival hyperplasia
  • Rituximab – hypogammaglobulinemia, infusion reactions
  • MMF – leukopenia, GI upset
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40
Q

AIN DDx

A
  • Drugs
    • NSAIDs, PPIs, penicillins and cephalosporins, fluoroquinolones/ciprofloxacin, rifampin, TMP-SMX, diuretics, allopurinol, indinavir, 5-ASA, cimetidine)
    • Eosinophils on bx
  • Infections
    • Legionella, Leptospira, cytomegalovirus (CMV), Streptococcus, Mycobacterium tuberculosis, Corynebacterium diphtheriae, Epstein-Barr virus (EBV), Yersinia, polyomavirus, Enterococcus, Escherichia coli, adenovirus, Candida, and others
    • Neutrophils on Bx
  • Autoimmune
    • SLE, Sarcoidosis, Sjögren’s syndrome, IgG4RD, hypocomplementemic tubulointerstitial nephritis, anti-tubular basement membrane (TBM) antibodies
    • Lymphocytes on Bx
  • TINU
    • Patients present with interstitial nephritis and uveitis and occasionally with systemic findings including fever, weight loss, fatigue, malaise, anorexia, asthenia, abdominal and flank pain, arthralgias, myalgias, headache, polyuria, and/or nocturia
    • Lymphocytic on Bx
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41
Q

Complications of nephrotic syndrome

A
  • Edema
  • VTE
  • Dyslipidemia
  • Infection / hypogammaglobulinemia
  • Protein malnutrition
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42
Q

Ways to prevent tumor lysis syndrome?

A
  • IV fluids (increase urinary flow rate)
  • Allopurinol (xanthine oxidase inhibitor, decrease uric acid pdn)
  • Rasburicase (do not use in G6PD deficiency; increase urate metabolism)
  • Hold ACE, nephrotoxins
  • No role for urinary alkalinization
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43
Q

What is PTU and renal side effects

A

Propylthiouracil

ANCA vasculitis, AIN

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44
Q

Cardiorenal syndrome types

A
  • Type 1 (acute) – Acute HF results in acute kidney injury
  • Type 2 – Chronic cardiac dysfunction (eg, chronic HF) causes progressive chronic kidney disease
  • Type 3 – Abrupt and primary worsening of kidney function due, for example, to renal ischemia or glomerulonephritis causes acute cardiac dysfunction, which may be manifested by HF.
  • Type 4 – Primary CKD contributes to cardiac dysfunction, which may be manifested by coronary disease, HF, or arrhythmia.
  • Type 5 (secondary) – Acute or chronic systemic disorders (eg, sepsis or diabetes mellitus) that cause both cardiac and renal dysfunction.
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45
Q

Causes of AKI after hematopoeitic stem cell tx

A
  1. Prerenal, post-HCT capilary leak syndrome
  2. ATN secondary to ABx while pancytopenic
  3. CNIs (used to prevent GVHD)
  4. Hepatic sinusoidal obstruction syndrome (venoocclusive disease - chemoradiation-induced hepatic sinusoidal endothelial cell injury, which results in sinusoidal thrombosis and obstruction and portal hypertension)
  5. TMA
  6. Engraftment syndrome (presents like cytokine storm)
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46
Q

Classic features of HSP/IgAV

A
  • Clinical feature - classic tetrad:
    • Palpable purpura without thrombocytopenia and coagulopathy - leukocytoclastic vasculitis, predominant IgA
    • Arthritis/arthralgia - oligo, migratory
    • Abdominal pain
    • Renal disease - IgA
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47
Q

Pathologic findings of IgA that worsen prognosis

A

MEST-C

Glomerulosclerosis, IFTA, fibrous crescents

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48
Q

Poor clinical markers of IgA nephropathy

A

HTN >140/90

Proteinuria >1g/d

High Cr at presentation

Smoking, obesity

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49
Q

Causes of secondary IgA nephropathy

A

IBD

Celiac disease

Cirrhosis

RA

Sarcoidosis

HIV

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50
Q

Causes of urate nephropathy

A
  • TLS
  • Gout (more chronic urate nephropathy)
  • Tissue catabolism (seizures, treatment of solid tumor)
  • Fanconi syndrome (uricosuria)
  • Lesch-Nyhan syndrome (primary overproduction of uric acid due to hypoxanthine-guanine phosphoribosyltransferase deficiency
  • IBD
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51
Q

Chemotherapy drugs and mechanism of AKI

A
  • Cisplatin (and carboplatin though less) - ATN, TMA, Fanconi
  • Cyclophosphamide - hemorrhagic cystits
  • Ifosfamide - hemorrhagic cystitis, prox RTA, distal RTA
  • Gemcitabine - TMA
  • Methotrexate - ATN, prerenal
  • 5-Fluorouracil - prerenal AKI
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52
Q

4 renal disease that cause fibrils on biopsy

A

AL Amyloid amyloidosis (10-12nm)

Fibrillary glomerulonephritis (10-20nm)

Immunotactoid glomerulopathy (20-80nm)

Cryoglobulinemic MPGN Type I (30-40nm)

53
Q

Pathology of PIGN

A
  • LM: Diffuse, proliferative and exudative GN with endocapillary proliferation and neutrophils.
  • IF: C3 and IgG in a dufuse, granular pattern within mesangium and capillary walls (“starry sky”)
  • EM: Subepithelial deposits shaped like “humps”
54
Q

Secondary causes of FSGS

A
  • Genetic: mutations in podocin, alpha-actinin 4, WT-1, CD2AP, TRPC6, mitochondrial cytopathies
  • Viral-related: HIV, parvovirus B19
  • Drug-related: heroin, inteferon-alfa, lithium, pamidronate, anabolic steroids
  • Reduced nephron mass/hyperfiltration: oligomeganephronia, unilateral renal agenesis, renal dysplasia, reflux nephropathy, secondary to surgical or traumatic ablation, chronic allograft nephropathy
  • Other: obesity, hypertension, atheroembolic, cyanotic congenital heart disease, sickle cell disease, Hodgkin’s disease, NH lymphoma
55
Q

Treatment of primary FSGS

A
  • Steroids
  • CNI
  • MMF
  • CYC or RTX
  • +/- PLEX..
56
Q

Indications for hemodialysis with Lithium

A
  • CNS symptoms (seizures, decreased LOC), irrespective of lithium level
  • Lithium >5 mmol/L
  • Lithium >4 with Cr >150
  • Lithium >2.5 with symptoms of lithium toxicity
57
Q

When to stop hemodialysis for lithium

A

Level <1 (at 6-8hr post dialysis to ensure no rebound)

58
Q

Management of toxic alcohol poisoning

A
  • Fomepizole (or alcohol)
  • Cofactors - folic acid (methanol), thiamine and B1 (ethylene glycol)
  • Bicarb - decrease active toxic metabolite by increasing pH
  • Dialysis
59
Q

Indications for fomepizole on toxic alcohol poisoning?

Indications for dialysis?

A
  • Fomepizole
    • Clear hx of ingestion of EG or M
    • Osm gap >10
    • EG level >3.2
    • Methanol level >6.2
  • Dialysis:
    • Coma/seizures
    • pH 7.15 AND EG >8.1 or M >15.6
    • Target organ damage (AKI, visual disturbance)
    • AKI
    • High AG
60
Q

Diuretic resistance in nephrotic syndrome?

A
  • increased diuretic volume of distribution
  • drug-binding to filtered protein in tubule fluid
  • strong primary stimulus to NaCl retention
61
Q

Causes of refractory edema

A
  • Inadequate diuretic dose or frequency
  • Decreased gut absorption
  • Decreased diuretic seceretion into tubular fluid
    • (diuretics are protein-bound so hypoalbuminemia will reduce delivery)
  • Increased sodium reabsorption distal to site of diuretic
  • Excess sodium intake
  • Drug interaction with diuretic action
    • (NSAIDs decrease GFR, thiazolidinediones increase ENaC and proximal sdium reabsorption)
62
Q

4 ways hypercalcemia can cause AKI

A

Vasoconstriction

Hypovolemia (inhibit CaSR LoH and collectin duct)

Stones from hypercalciuria

Nephrocalcinosis

63
Q

What diseases cause linear IgG staining?

A

Anti-GBM

Diabetic nephropathy

Light chain deposition disease

Fibrillary GN

64
Q

Indications for immunosuppressive therapy for membranous nephropathy?

A
  • Very high risk - treat right way:
    • Any 2 of, at the time of diagnosis:
      1. Cr >=133
      2. GFR decrease >25% in last 2 yrs
      3. Life-threatening nephrotic sx (Alb <20-bromocresol purple or <25-bromocresol green, refractory edema, or VTE)
  • High risk - over observation period of 3-6 mo’s:
    • Any 2 of:
      1. GFR decrease >=25% at any time during obs
      2. Proteinuria >8g/d x 6 months
      3. PLA2rAb >150 RU/mL
65
Q

Mechanisms of post-obstructive diuresis?

A
  • Pressure naturesis due to resolution of salt- and water-retention
  • Loss of medullary concentrating gradient (decreased ability for NKCC)
  • Tubular injury with partial nephrogenic DI (downregulation of aquaporins)
  • Osmotic diuresis (urea)
  • Secretion of diuretic factors (ANP) during obstruction
  • Increased prostaglandin synthesis with relief of obstruction (hence afferent vasodilation and increased GFR)
66
Q

4 ways to prevent AKI with contrast?

A
  1. Maintain euvolemia
  2. Avoid nephrotoxic agents eg. NSAIDs
  3. Use iso-osmolar contrast
  4. Use lowest dose of contrast possible
67
Q

Drug causes of MCD

A

NSAIDs

Antimicrobials: ampicillin, cephalosporins, rifampin

Bisphosphonates

Sulfasalazine, 5-ASA derivatives

Penicillamine

Lithium

68
Q

Clinical presentation of urogenital TB?

A
  • Urinary collecting system
    • Segmental ureteric strictures, segmental dilatations (“corkscrew” ureter), or shortened rigid ureter (“pipe-stem” ureter)
    • Dystrophic calcification -> “cement kidney”
    • Unilateral involvement more common
  • Kidney
    • AIN, GN, amyloidosis
69
Q

Define Type I, II, and III cryoglobulins

A
  • Type I
    • Monoclonal Ig’s (either IgG or IgM)
  • Type II
    • Polyclonal IgG and monoclonal IgM (this IgM has RF activity)
  • Type III
    • Mixture of polyclonal IgM and IgG’s
70
Q

Meltzer triad?

A

Purpura

Arthralgias

Weakness

(Cryoglobulinemia)

71
Q

Causes of cryoglobulinemia

A

Infection: HepC, HepB, HIV

Autoimmune: Sjogren’s, SLE, RA

Malignancy: B-cell lymphoma, MM

72
Q

Anti-GBM disease after transplantation in Alport’s disease - how often does this occur and why?

Incidence of graft loss in these patients?

A

<5%

Alport’s have a defect in their type IV collagen, leading to an altered Goodpasture antigen. The donor kidney has a normal antigen that was previously “unseen” by the recipient, potentially causing an immune response -> anti-GBM antibodies.

Of those who get anti-GBM, ~75% lose graft

73
Q

Treatment for Anti-GBM

A
  1. Plasmapheresis daily x 14 days until anti-GBM negative
    1. 60mL/kg ~4L exchanges per day, replace with albumin (or FFP is biopsy/bleeding)
  2. Pulse steroids
  3. Cyclophosphamide po 2mg/kg (adjust for age and GFR) x 3 months

Consider NO treatment if dialysis-dependent at presentation, 100% crescents, and no pulmonary hemorrhage… depends

74
Q

ISN/RPS classification of lupus

A
  • Class I – Minimal mesangial LN
    • LM: normal
    • IF/EM: mesangial immune deposits
  • Class II – Mesangial proliferative LN
    • LM: Mesangial hypercellularity and/or expansion
    • IF/EM: mesangial immune deposits
  • Class III – Focal LN
    • LM: Segmental or global endocapillary or extracapillary GN, <50% of glomeruli
    • IF/EM: Mesangial and subendothelial immune deposits
  • Class IV – Diffuse LN
    • LM: Segmental or global endocapillary or extracapillary GN, >50% of glomeruli
    • IF/EM: Mesangial and subendothelial immune deposits
  • Class V – Membranous nephropathy
    • LM: GBM thickening
    • IF/EM: Mesangial and subepithelial immune deposits
  • Class VI – Advanced sclerosing LN
    • >90% glomeruli globally sclerosed without residual disease activity
75
Q

Treatment options for proliferative lupus nephritis

A
  1. Steroids + MMF
  2. Steroids + low-dose CYC (EUROLUPUS)
  3. Steroids + high-dose CYC (NIH)
  4. Steroids + oral CYC
  • Methylpred 500mg-1g/day x 1-3 days -> prednisone 1 mg/kg/d (max 80mg/d), taper over several weeks
  • MMF 2-3 g/day x 6- months (preferred in child-bearing age, African or Hispanic descent)
  • Low-dose CYC (EUROLUPUS): CYC IV 500 mg q2wk x 3 months/6 doses
  • High-dose (NIH): CYC IV 500mg-1 g q1month x 6 months
  • Oral CYC 1-1.5 mg/kg/day (max 150 mg/d) x 2-4 months
76
Q

Risk factors for aminoglycoside nephrotoxicity?

A
  • Age
  • Pre-existing CKD
  • Concurrent nephrotoxic agents eg. NSAID
  • Prolonged duration of therapy
  • Supratherapeutic level of drug
  • Sepsis
  • Volume depletion
77
Q

Causes of hemoglobinemia/hemoglobinuria?

A

Mechanical valve/shear stress

TTP/HUS

Hemolytic transfusion reaction

PNH

RBC destruction from toxins (Clostridium, snake bites)

Osmotic lysis from hypertonic saline

78
Q

How does midodrine work and 2 indications for use?

A

Alpha-1-adrenergic agonist which increases arteriolar and venous tone

Indications:

  1. Refractory intradialytic hypotension
    1. Limits intradialytic hypotension when used at a dose of 10mg PO 30 minutes-2hours before dialysis session.
    2. Dose-limiting factor is supine hypertension
    3. Contraindicated if active cardiac ischemia
  2. Hepatorenal syndrome
    1. Combined with octreotide, improves renal and systemic hemodynamics
79
Q

Difference between c-ANCA vs. p-ANCA?

A
  • In vasculitis, the two relevant target antigens are proteinase 3 (PR3) and myeloperoxidase (MPO) which are located in the granules of neutrophils and lysozymes. Both PR3 and MPO are located in the azurophilic granules of neutrophils and the peroxidase-positive lysosomes of monocytes.
  • cANCA: staining is diffuse throughout the cytosplams, Ab are directed against PR3 (occasionally MPO)
  • pANCA: stainining is around the nucleus (peri-nuclear), Ab are directed against MPO (occasionally PR3)
80
Q

Diseases associated with +p-ANCA?

A
  • MPA
  • EGPA
  • Drug-induced ANCA vasculitis (PTU, Methimazole, Hydralazine, Minocycline, Levimasole-contamined cocaine)
  • Renal-limited vasculitis
  • ANCA+ anti-GBM disease
  • Other non-vasculitic causes:
    • Rheum
    • Autoimmune GI (UC, PSC)
    • Cystic fibrosis
81
Q

Medications that can cause nephritic syndrome

A

AAV: PTU, methmiazole, hydralazine, minocycline, levimasole

Lupus: Hydralazine, procainamide, quinidine, penicillamine, Anti-TNF (infliximab, etanercept), etc.

82
Q

Side effects of cyclophosphamide

A
  1. Infertility
  2. Opportunistic infections
  3. Bladder cancer
  4. Hemorrhagic cystitis
  5. Teratogenicity
  6. Nausea
  7. Hair loss
  8. Hematologic: thrombocytopenia, anemia, leukopenia
83
Q

Mortality of patient requiring dialysis in the ICU?

Renal factors associated with mortality in the ICU?

Dialysis-related factors associated with ICU mortality?

A
  • Patients requiring dialysis in the ICU - mortality rates 40-60%
  • Renal factors:
    • Dialysis-requirement
    • Oliguria
    • Cr >177?
  • Dialysis-related factors:
    • ???
84
Q

Causes of TMA

A
  • Idiopathic TTP (ADAMSTS13 deficiency)
  • HUS (Shiga-toxin producing e.coli)
  • Atypical HUS/Complement mediated
  • Systemic conditions associated with TMA:
    • Pregnancy - pre-eclampsia, HELLP
    • Autoimmune - APLA, scleroderma renal crisis
    • Infection - HIV
    • Malignant Hypertension
    • DIC
    • Malignancy
  • Drug-induced - see other card
85
Q

Drugs that cause TMA

A
  1. Cyclosporine
  2. Tacrolimus
  3. Ticlopidine
  4. Clopidogrel
  5. Quinine
  6. Mitomycin C
  7. Gemcitabine
  8. Cisplatin
  9. Oxaliplatin
  10. Pentostatin
  11. Bevacizumab
  12. Sunitinib
86
Q

Common causes of microscopic hematuria in 32 year-old

A

Non-glomerular: transient (exercise, fever), UTI

Glomerular: IgA, thin basement membrane

87
Q

Non-traumatic causes of rhabdomyolysis

A
  • Exertional/normal muscle: extreme exertion, heat illness, seizures
  • Exertional/abnormal muscle: metabolic myopathies, mitochondrial myopathies, malignant hyperthermia, NMS
  • Non-exertional:
    • Medications: Statins
    • Drugs of abuse: Heroin, cocaine, methamphetamines, methadone
    • Exposures: Snake venoms, carbon monoxide, mushroom poisoning
    • Infections: Influenza, Coxsackievirus, EBV, HSV, Parainfluenza, Adenovirus, HIV, CMV, etc…
    • Metabolic: Hypokalemia, Hypophosphatemia, Hypothyroidism
    • Inflammatory myopathies: dermatomyositis, polymyositis
88
Q

4 renal effects of sarcoidosis

A
  1. Hypercalcemia
    1. Vasoconstriction -> prerenal AKI
    2. Nephrogenic DI
  2. Hypercalciuria
    1. Stones, nephrocalcinosis
    2. Distal RTA
  3. Acute/chronic interstitial nephritis with granulomas
  4. Associated with other GNs (rare): IgA nephropathy, membranous nephropathy
  5. Retroperitoneal lymph node involvement/fibrosis → post-renal obstruction
  6. Central DI → polyuria and electrolyte abnormalities
89
Q

Renal effects of lithium

A
  1. Nephrogenic diabetes insipidis
  2. Distal RTA
  3. Chronic interstitial nephritis
  4. Nephrotic syndrome - MCD, FSGS
  5. Idiopathic edema during manic phase
  6. Hyperparathyroidism with hypercalcemia and hypercalciuria (with AKI) - due to increased CaSR sensitivity in parathyroid gland
  7. (?possible interaction with ACE inhibitors leading to renal insufficiency - just need to monitor closely)
90
Q

Diagnostic tests for calciphylaxis

A

Bone scan for extraosseous calcification

Skin biopsy

91
Q

Causes of GN with low complement

A
  1. Lupus nephritis - low C3 and C4
  2. PIGN - low C3
  3. Complement-mediated TMA - low C3
  4. MPGN - low C3
  5. Other kidney diseases:
    1. Cholesterol emboli syndrome
    2. Cirrhosis/HRS (decreased production of complements)
92
Q

Timing of GN for:

IgA?

PIGN post-strep pharyngitis?

PIGN post-strep skin infection?

PIGN post-staph skin infection?

A

IgA - synpharyngitic <5 days

PIGN post-strep pharyngitis - 1-3 weeks

PIGN post-strep skin infection - 3-6 weeks

PIGN post-staph infection - can be shorter than strep pharyngitis, can be IgA dominant, more common diabetics/comorbid

93
Q

DDx pulmonary-renal syndrome

A
  1. AAV: GPA, EGPA, MPA, Drug-induced
  2. Anti-GBM
  3. Immune-complex: SLE/APLAS, IgA, Cryo, RA vasculitis
  4. Other disease causing pum/renal problems - TTP, cardiorenal, severe pneumonia with PIGN, ARDS with AKI, paraquat poisoning
94
Q

Clinical manifestations of GPA

A
  1. Nasal/oral inflammation
    1. Oral ulcers, prurulent or bloody nasal discharge, nasal crusting, sinusitis, otitis media, otorrhea, conductive and sensorineural hearing loss
  2. Bony/cartilage destruction
    1. saddle nose deformity, upper airway and orbital masses, cranial nerve entrapment
  3. Abnormal CXR with respiratory symptoms
    1. nodules, airspace disease cavities → SOB, cough, hemoptysis, pleuritc pain, SOB
  4. Glomerulonephritis
  5. C-ANCA (PR3) positive in 70%
  6. Granulomatous inflammation on bx of artery
95
Q

5 strategies to prevent/manage steroid-induced osteoporosis?

A
  • Ca and Vit D
  • Bisphosphonate, denosumab if GFR >30
  • Limit dose of steroid required
  • Utilize steroid-sparing immunosuppressive agents
  • Weight-bearing exercises
96
Q

Dysproteinemias and ways it can cause kidney disease

A
  1. Glomerular
    1. AL amyloidosis
    2. Light chain deposition disease
    3. Heavy chain deposition disease
    4. Fibrillary glomerulonephritis
    5. Immunotactoid glomerulopathy
    6. MPGN, cryoglobulinemia
  2. Tubulointerstitial
    1. Light chain cast nephropathy ‘myeloma kidney’
    2. Fanconi’s syndrome
    3. Interstitial nephritis
  3. Other
    1. Hypercalcemia (many renal effects)
    2. Waldenstom Macroglobulinemia with hyperviscosity
97
Q

IV recreational drugs that can cause renal disease

A
  • Heroin (FSGS)
  • Cocaine (Drug-induced ANCA if contaminated with levimasole, Malignant hypertension)
  • Methamphetamines (Malignant hypertension)
  • MDMA (hyponatremia)
  • HIV (Collapsing FSGS, Lupus-like proliferative GN, IgA)
  • HepC (MPGN-Immune Complex associated with cryoglobulinemia, Membranous nephropathy)
  • HBV (MPGN-Immune Complex, Membranous nephropathy)
  • Endocarditis (PIGN, MPGN-Immune Complex)
98
Q

Indications for PLEX

A
  1. Anti-GBM
  2. TTP
  3. Complement-mediated TMA
  4. Cryoglobulinemia/hyperviscosity syndrome
  5. Catastrophic APLA
  6. Antibody-mediated rejection
  7. Desensitization pre-transplant
99
Q

HCV and related kidney diseases

A
  1. Type 1 MPGN as a consequence of essential mixed cryoglobulinemia (Classic)
  2. Membranous Nephropathy
  3. Polyarteritis nodosa (ATN/renal infarct due to arteritis)
  4. If coinfection with HBV → membranous
  5. If coinfection with HIV → collapsing FSGS
  6. If diabetes → may precipitate progression
  7. Also reported cases: IgA nephropathy, FSGS, Fibrillary glomerulonephritis, Immunotactoid
100
Q

Non-renal manifestations of nephrotic syndrome

A

1) Hypoalbuminemia
2) Hyperlipidemia (hypertriglyceridemia)
3) Hypercoagulability
4) Infection
5) Edema

101
Q

Mesangial staining on IF

A

IgA

Lupus nephritis class I and II

MPGN

MIDD

102
Q

Difference in biopsy findings for amyloidosis, fibrillary, immunotactoid, cryo?

A
  • Amyloidosis - deposits are pale PAS-, Congo Red+, light chain restricted, fibrils are random and 8-12nm
  • Fibrillary - deposits are PAS+, Congo Red-, polyclonal, fibrils are random and 10-20 nm
  • Immunotactoid - light-chain restricted, microtubular structure (rather than randomly-oriented fibrils) and 20-80nm
  • Cryo - PAS+ deposits (pseudothrombi) microtubules 30-40nm, fingerprint pattern
103
Q

Causes of mesangial proliferation and positive IF

A
  • With nodules:
    • 1) Diabetic nephropathy
      • Linear IgG, Kappa>Lambda
    • 2) Light chain deposition disease
      • Linear Kappa or Lambda
    • 3) MPGN1
      • Granular IgG, IgM, C3
  • Without nodules
    • 1) Mesangial lupus nephritis (Class II)
      • Granular IgG, IgM, IgA, C3, C1q (“full house”)
    • 2) IgA nephropathy
      • Granular IgA, often C3 at high intensity and IgG/IgM at low intensity, Lambda>Kappa
    • 3) PIGN
      • Granular IgG, C3, often IgM
104
Q

Indications to treat UPJ obstruction?

When would you not treat it?

A
  • UPJ obstruction common in children, may be incidental finding in adult or due to stones/tumor/fibrosis/stricture. Treatment options include surveillance vs. surgery
  • Indications to treat:
    • Recurrent infection
    • Recurrent stones
    • Decline in renal function attributed to obstruction
    • Post-pyelonephritis (don’t fix during infection)
  • Don’t treat if:
    • Asymptomatic
    • Normal renal function or irreversible damage
    • No recurrent stone formation or severe infections
105
Q

Risk factors for hospital-acquired/nosocomial UTI?

A
  1. Broad spectrum antibiotics increase risk of fungal infections
  2. Urologic procedure
  3. Indwelling catheter
  4. Long hospitalization
  5. Structural/functional abnormalities (neurogenic bladder)
  6. Women
  7. Diabetes (including use of SGLT2 inhibitors)
  8. Malnutrition
106
Q

Indications for rituximab

A

Membranous nephropathy, primary

MCD

AAV

Transplant ABMR

Other: FSGS, LN, TTP, MPGN, PTLD

107
Q

2 renal factors associated with mortality in ICU

A

dialysis requirement

oliguria

Cr >177

108
Q

Risk factors for contrast-induced nephropathy

A
  1. Preexisting renal dysfunction (Cr>132)
  2. Volume depletion or decreased effective circulating volume (cirrhosis, CHF)
  3. Large volume radiocontrast
  4. High osmolar radiocontrast
  5. Arterial contrast administration
  6. Concomitant treatment with ACEi, NSAIDS, exposure to other nephrotoxins
  7. Diabetic nephropathy with renal insufficiency (not diabetes alone)
109
Q

Prevention of contrast induced nephropathy

A
  1. Keep euvolemic
  2. Prefer iso-osmolar or low-osmolar contrast (vs. high-osmolar contrast)
  3. Lowest volume contrast possible
  4. Avoid repeat contrast exposure within 48 hours
  5. Avoid contrast if possible
  6. Avoid nephrotoxic agents
110
Q

5 renal diseases that can occur with bacterial endocarditis

A
  • PIGN [MPGN immune complex, mesangioproliferative] (peaks just before therapy starts)
  • Cholesterol emboli with valve replacement
  • Septic emboli- renal infarcts
  • Drug-induced AIN with penicillin, cephalosporin, quinolone (after >10 days of treatment)
  • Embolic renal infarction (months after bacteriologic cure)
  • Renal abscess
  • ATN (Sepsis, Aminglycosides)
  • Pre-renal from HF
111
Q

Woman, DM1, RA, Sjogrens, dermatitis herpetiformis, chronic NSAID with AKI, 5 RBCs, 5 WBCs, no casts, subnephrotic proteinuria. 5 causes

A
  • AIN/CIN sjogrens
  • AIN/CIN NSAIDS
  • Pre-renal from NSAIDS on underlying DM nephropathy
  • IgA (dermatitis herpetiformis)
  • MPGN, membranous (RA)
112
Q

Work-up for sarcoidosis and management?

A
  • Work-up
    • PTH, Vitamin D (including activated VitD), ACE
    • CXR
    • PFTs
    • Urinalysis, renal u/s
    • CT thorax with biopsy (LN or kidney)
  • Treatment of this case:
    • If no extrapulmonary involvement, treatment is conservative with monitoring of CXR, PFTs
    • Treatment of ocular, neurologic, myocardial, or renal sarcoidosis or hypercalcemia is indicated even when symptoms are slight, because severe loss of vision, fatal arrhythmias, or insidious renal damage may ensue
    • Treat hypercalcemia with aggressive IVF
    • High dose steroids for 6 weeks, then tapered to a maintenance dose to complete 1 year of treatment
113
Q

Renal diseases associated with RA

A
  1. Drugs: NSAIDS (Minimal change/AIN), Gold (Membranous nephropathy), Penicillamine (Membranous nephropathy)
  2. Rheumatoid vasculitis
  3. Secondary AA amyloid
  4. Associated with other GNs (rare): MPGN (Immune complex), Membranous nephropathy, IgA nephropathy
  5. DM Nephropathy
114
Q

Renal manifestations of Sjogren’s

A
  1. Interstitial nephritis
  2. Distal Type 1 RTA
  3. Nephrogenic DI
  4. Hypokalemia from tubular injury in interstitial nephritis
  5. Secondary AA Amyloid
  6. Associated with other GNs (rare): MPGN (Immune complex), Membranous nephropathy
115
Q

Prevention of HRS

A

1) IV albumin in SBP: 1.5g/kg on day 1, 1.0g/kg on day 3 (decreased HRS and survival advantage)
2) Norfloxacin in ascites if any of: Child-Pugh>9 and Bili>51.3, Cr>106, BUN>20, Na<130 (decreased HRS and survival advantage)

116
Q

5 drug classes that can cause AIN

A
  1. NSAIDS
  2. Penicillins
  3. Cephalosporins
  4. Fluoroquinolones
  5. Sulfa drugs (tmp-smx)
  6. PPI
  7. Rifampin, Indinavir
  8. Cimetidine
  9. Allopurinol
  10. 5-ASA
117
Q

Management of AIN

A

1) Discontinue offending drug
2) If no significant improvement after 3-7 days of discontinuation of the offending agent and if biopsy proven and no significant chronic damage, trial steroids: 1mg/kg for 2 weeks with taper for total duration of 3 months NSAID induced interstitial nephritis often steroid-resistant

118
Q

Risk factors for AKI from NSAIDs

A

1) Preexisting chronic kidney disease
2) Volume contraction, decreased effective circulating volume (cirrhosis, nephrotic syndrome, CHF, sepsis) or diuretic use
3) Other drugs that affect renal blood flow: RAS blockers, CNIs
4) Duration and dose of NSAID exposure
5) Elderly

119
Q

Renal syndromes associated with NSAIDs

A
  1. Hemodynamically mediated AKI (Prerenal or increased risk of ATN if other insults)
    1. Due to inhibition of prostaglandin synthesis (which usually acts to preserve renal blood flow by vasodilation at afferent arteriole during hypovolemia) causing reversible renal ischemia, decline in glomerular hydrostatic pressure, and AKI Increased Cr at 3-7 days
  2. Acute interstitial nephritis
  3. Minimal change disease (→ Nephrotic syndrome)
    1. May coexist with interstitial nephritis
  4. Membranous nephropathy
  5. Papillary necrosis (Chronic kidney disease from prolonged use)….other = sickle cell, analgesia, pyelo, dm
  6. Sodium retention exacerbating hypertension and CHF (inhibit normal effect of PG on sodium reabsorption)5
  7. Hyponatremia (inhibit normal effect of PG on ADH)
  8. Hyperkalemia (inhibit ang II induced aldosterone release and lower renin)
  9. HTN
120
Q

3 causes of AKI and/or increased Cr due to Septra

A
  1. Decreased secretion of Cr
    1. Trimethoprim inhibits tubular creatinine secretion
  2. AIN
    1. sulfamethoxazole
  3. Crystal nephropathy and tubular damage
    1. sulfamethoxazole, insoluble in acid urine
121
Q

Drugs that increase creatinine without affecting GFR

A
  • Decreased secretion of Cr
    • Trimethoprim
    • Cimetidine
    • Tyrosine kinase inhibitors (eg. imatinib)
    • Dronedarone
  • Interference with serum assay
    • Flucytosine
    • Cefotixin
    • IVIG
  • Others…
    • Fenofibrate
    • Salicylates
122
Q

How does aminoglycoside nephrotoxicity usually present?

A
  • Onset at 5-7 days
  • Distal tubular dysfunction
    • initially concentrating defect manifested as polyuria (decreased sensitivity to ADH)
  • Non-oliguric AKI with FeNa >1%
  • Reversible progressive loss of kidney function, lag until recovery after drug discontinued due to accumulation in renal cortical tissue. Complete recovery within several weeks.
  • Bland urinalysis
  • Fanconi-like syndrome: Urinary phosphate and magnesium wasting (magnesium depletion leads to hypokalemia and hypocalcemia)
123
Q

Electrolyte abnormalities with aminoglycoside nephrotoxicity?

A
  1. Hypophosphatemia (Fanconi-like proximal tubular dysfunction)
  2. Hypomagnesemia (Impaired magnesium reabsorption in TAL of loop of henle)
  3. Hypokalemia (due to hypomag)
  4. Hypocalcemia (due to hypomag)
124
Q

Features that suggest diagnosis other than DM nephropathy

A
  • Onset of proteinuria < 5 years from the onset of DM1
  • Absence of retinopathy in DM1
  • Acute onset of renal disease (rapidly declining GFR)
  • Signs and symptoms of another systemic disease
  • Active urine sediment containing RBC and cellular casts (hematuria and RBC casts may be seen in DN)
125
Q

Causes of papillay necrosis?

IVP findings?

A
  1. Causes of papillary necrosis (sequelae of ischemia occurring in the renal papillae and medulla)
    1. Diabetes
    2. Pyelonephritis
    3. Obstruction
    4. Sickle Cell anemia
    5. NSAIDS
    6. Renal TB
  2. IVP Findings in Papillary Necrosis
    1. Ureteral filling defects, blunted calyces, sloughed papillae
    2. Small kidneys
126
Q

3 causes of nodular glomerulopathy not diabetic

A

Amyloid

MIDD

Fibrillary

Immunotactoid

127
Q

Risk factors for TLS?

A
  • Rapidly dividing tumors and hematological malignancies higher risk
  • Large tumor burden
  • Highly responsive tumors to therapy
  • Preexisting CKD or AKI, nephrotoxins, oliguria, or acidic urine
  • Preexisting hyperuricemia or hyperphosphatemia
  • Preexisting volume depletion
128
Q

IgG4 disease - renal manifestations?

A
  • TIN
  • Membranous
  • Papillary necrosis
  • Inflammatory cysts
  • Retroperitoneal fibrosis

Hypocomplementemia

Eosinophilia

N (8 decks)

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