Renal Flashcards
What are four criteria of nephrotic syndrome?
1) peripheral edema
2) hypoalbuminemia < 2.5 g/dl
3) proteinuria > 3.5gm in 24 hours; 2gm on spot urine protein/creatinine
4) hyperlipidemia
What are the main tests you’ll send for assessing nephrotic syndrome? name 6 tests
- 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.
Leading cause of nephrotic syndrome in the US?
diabetes
Name a few diagnoses of nephrotic syndrome after DM in the US?
membranous (hep B)
FSGS (think HIV)
minimal change disease (think peds)
Why does edema happen in nephrotic syndrome? Name two hypothesis
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).
What are the main management approaches for nephrotic syndrome?
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
What is the prognosis and mgmt of diabetic nephropathy?
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.
What is prognosis and mgmt of minimal change disease?
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).
What is the prognosis and mgmt of FSGS?
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.
What is prognosis and mgmt of membranous nephropathy?
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.
What are the 3 elements of GN?
- AKI
- Hypertension
- Hematuria/Proteinuria/Pyuria
What are the three big buckets of rapidly progressing GN diagnosis?
- Pauci immune GN: ANCA associated small vessel vasculitis
- Anti-glomerular basement membrane (GBM): autoantibodies against the glomerular basement membranes
- Immune complex GN: lupus nephritis (has wide range of presentations), IgA nephropathy, membranoproliferative, post-infectious
What is CKD stage 3 defined as?
GFR < 60; 3a 45-59; 3b 30-44
When should you refer to a specialist for CKD?
GFR < 30; CKD stage 3b going to 4
persistent proteinuria > 300 mg/g
What is goal Hgb in CKD patients?
10-11, don’t overshoot!
How to treat Hgb in CKD patients? What do we check?
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
What are most common obstruction cases of AKI?
cjhildren: anatomic; young adults: kidney stones; older adults- prostatic, kidney stones
Hematuria w/o RBCs…think…
myoglobin/rhabdo
