Renal

Question 1

What are four criteria of nephrotic syndrome?

Answer 1

1) peripheral edema
2) hypoalbuminemia < 2.5 g/dl
3) proteinuria > 3.5gm in 24 hours; 2gm on spot urine protein/creatinine
4) hyperlipidemia

Question 2

What are the main tests you’ll send for assessing nephrotic syndrome? name 6 tests

Answer 2

• SPEP/UPEP (multiple myeloma)
  
  • ANA (lupus)
  • hepatitis C serology (Membranoproliferative glomerulonephritis, cryoglobulinemia)
  • hepatitis B serology (membranous nephropathy)
  • HIV screening (collapsing FSGS),
• and anti-PLA2R (idiopathic membranous nephropathy).
  An anti-phospholipase A2 receptor (PLA2R) titer measures autoantibodies responsible for 70-80% of idiopathic membranous nephropathy. The test was identified in 2009 and can be used for diagnosis, prognosis and monitoring in patients with idiopathic membranous nephropathy(Beck et al 2009). In addition to labs aimed at evaluating the etiology of NS, Dr. Topf recommends a CBC and PT/PTT before a renal biopsy is completed.

Question 3

Leading cause of nephrotic syndrome in the US?

Answer 3

diabetes

Question 4

Name a few diagnoses of nephrotic syndrome after DM in the US?

Answer 4

membranous (hep B)
FSGS (think HIV)
minimal change disease (think peds)

Question 5

Why does edema happen in nephrotic syndrome? Name two hypothesis

Answer 5

Underfill hypothesis vs Overfill hypothesis (now leading hypothesis)

Underfill hypothesis: loss of albumin in the serum leads to decreased plasma oncotic pressure and increased fluid movement into the interstitium. The blood vessels are then “underfilled” leading to secondary sodium retention via activation of the renin-angiotensin-aldosterone system (RAAS).
Overfill hypothesis: primary renal sodium retention, independent of blood volume levels or albumin. Serum plasminogen gets activated to plasmin and this activates the epithelial sodium channel in the distal nephron to reabsorb sodium (Chen et al 2019). One line of evidence for the validity of the overfill hypothesis is the natural history of minimal change disease. Steroids result in rapid resolution of proteinuria and edema in minimal change disease. There is improvement in edema prior to increased albumin levels (Siddall & Radhakrishnan 2012).

Question 6

What are the main management approaches

Answer 6

1) edema - diuretics; 2) HL - statin until disease goes remission; 3) proteinuria - ACE/ARB; 4) diet - Na restriction; 5) consider AC - there is the UNC GN tool

Question 7

What is the prognosis and mgmt of diabetic nephropathy?

Answer 7

Diabetic nephropathy has a poor prognosis with loss of approximately 4-6ml/min of renal function per year, so in 10 years patients often progress to ESRD. The rate of decline can be improved with RAAS inhibition (Umanath & Lewis 2018) and SGLT2i.

Question 8

What is prognosis and mgmt of minimal change disease?

Answer 8

Minimal change disease: excellent prognosis with rapid response to steroids. There is a high rate of relapse but patients usually respond equally well to steroids during a relapse (KDIGO 2012).

Question 9

What is the prognosis and mgmt of FSGS?

Answer 9

variable prognosis with a 10-year risk of ESRD ranging from 40-70% and improved if remission is achieved (KDIGO 2012; Wehrmann et al 1990). Steroids, cyclosporine, and tacrolimus are used for treatment with variable response. Dr. Topf describes new experimental therapies that warrant referral to a center with available trial enrollment for interested patients.

Question 10

What is prognosis and mgmt of membranous nephropathy?

Answer 10

Dr. Topf describes how ~1/3 will have spontaneous remission, ~1/3 have lasting smoldering proteinuria with relatively stable renal function, and ~1/3 have aggressive progressive disease that requires treatment with cyclophosphamide and steroids.

Question 11

What are the 3 elements of GN?

Answer 11

1. AKI
2. Hypertension
3. Hematuria/Proteinuria/Pyuria

Question 12

What are the three big buckets of rapidly progressing GN diagnosis?

Answer 12

1. Pauci immune GN: ANCA associated small vessel vasculitis
2. Anti-glomerular basement membrane (GBM): autoantibodies against the glomerular basement membranes
3. Immune complex GN: lupus nephritis (has wide range of presentations), IgA nephropathy, membranoproliferative, post-infectious

Question 13

What is CKD stage 3 defined as?

Answer 13

GFR < 60; 3a 45-59; 3b 30-44

Question 14

When should you refer to a specialist for CKD?

Answer 14

GFR < 30; CKD stage 3b going to 4
persistent proteinuria > 300 mg/g

Question 15

What is goal Hgb in CKD patients?

Answer 15

10-11, don’t overshoot!

Question 16

How to treat Hgb in CKD patients? What do we check?

Answer 16

Check Iron studies including TSAT

• Low Hgb <10g/dl and transferrin sat (TSAT) <30 percent and ferritin <500ng/ml; Give IV Fe first, then EPO
• Hgb > 10g/dl and TSAT =>20 and ferritin > 200 ng/ml; Such patients are not treated with either iron or an ESA but continue to be monitored closely. Although patients may be considered anemic by World Health Organization (WHO) standards, they do not meet criteria for ESA therapy
• Hgb <10g/dl and TSAT > 30 percent; Such patients are usually started on an ESA, taking into consideration specific patient characteristics, such as functional and cognitive status, life expectancy, and other factors. Patients who have a history of stroke or malignancy or an active malignancy are important exception

Question 17

What are most common obstruction cases of AKI?

Answer 17

cjhildren: anatomic; young adults: kidney stones; older adults- prostatic, kidney stones

Question 18

Hematuria w/o RBCs…think…

Answer 18

myoglobin/rhabdo

Question 19

WBCs in UA

Answer 19

AIN, UTI, pyelo, sterile pyuria, contanminant in woman

Question 20

Low FeNa < 1%

Answer 20

typically pre-renal AKI; can also be ATN, contrast nephropathy, myoglubinuria, any cause of AKI where tubular function is preserved despite decreased glomurelar function

Question 21

When can we use in AKI dx with patient on diuretics?

Answer 21

Fe Urea

Question 22

When are hyaline casts seen vs waxy casts?

Answer 22

hyaline - poor perfusion; waxy - CKD

Question 23

AKI and urine sediment shows blood and protein

Answer 23

think GN – get renal involved

Question 24

contrast induced AKI - what score can be used to assess risk

Answer 24

in high risk patients - optimize renal perfusion prior to exposure 1ml/kg/hr for 6-12 hours

Mehran Score

Question 25

what should you do if pt with CKD needs a PICC?

Answer 25

alternative otions for IV access

consult nephrology to assess need for fistula placement

Question 26

what is threshold for phosphate binder?

Answer 26

if phosphorus remains > 5.5

sevelamer 800mg TID with meals

Question 27

If Vit D < 12, what do yo udo?

Answer 27

50U vid d2 for 8 weeks, then vitamin d3 daily 1000U

Question 28

with concern for infection in patient with tunneled dialysis catheteer, what blood cultures do you get?

Answer 28

get peripheral cultures, and additional set of blood cultures from dialysis catheter

Question 29

what kind of solution is used to treat catheter assoc infection when catheter not removed

Answer 29

antibiotic catheter LOCK solution good for GNR, less effective for GP infection

Question 30

Anemia in CKD - when to do IV Fe

Answer 30

If Hgb < 10, TSAT < 30