Nephro Flashcards
When to workup a HTN patient for FMD-related renal artery stenosis?
– Age <30, especially non-obese women
– HTN resistant to ≥3 drugs
– Kidneys asymmetrical (>1.5cm difference)
– Abdominal bruit but no atherosclerosis risk factors
– Confirmed FMD in another vascular bed
– Family hx of FMD
CTA is test of choice
Once FMD is confirmed:
– Screen vasculature from head to pelvis with either CTA or MRA (cervicocephalic lesions, brain aneurysms, lesions in other vascular beds).
Who to consider SBP target <120 according to SPRINT?
SPRINT candidates: consider intensive therapy (overlaps with high-risk)
– Age≥50 with clinical/subclinical CVD, eGFR20-60, protein<1g/day, 10-year CV risk≥15%
– Age≥75 alone is enough
– Caution in DM, previous stroke, eGFR<20, protein>1g/day (not studied/excluded fromSPRINT)
– Contraindications: non-adherence, standing SBP <110, 2o HTN, can’t measure BP accurately
– SBP ≥130
Options for SPC for treating HTN?
ACEi + CCB (Grade A);
ARB + CCB (B);
ACEi/ARB +diuretic (B)
What is the preferred anti-HTN combo post stroke?
Combination ACEi and thiazide preferred 1st line (Grade B)
When would stenting be considered in renovascular HTN?
Stenting may be considered if ANY 3 of the following present:
– uncontrolled BP on maximal therapy (4 or more drugs)
– progressive renal function decline
– OR acute pulmonary edema
When to use statin in Non-DM with HTN?
Statin if HTN + ≥3 vascular risk factors
3 populations to consider Ritux over Cyclophosphamide when treating ANCA vasculitis
– Pre-menopausal woman
– Men interested in preserving fertility
– Relapsed/refractory disease
Which GN presents with low C3?
Post Strep GN
Diagnosis: low C3, normal C4, +ASOT (70%), +anti-DNase B (90%). 2-3 weeks post infection.
Which GN presents with low C4?
MPGN
Associated with HCV, cryos, infection, cancer, complement dysregulation
Management: treat the underlying cause
-if idiopathic, treat like it’s proliferative lupus (steroids, and MMF or cyclophosphamide)
Which GN presents with low C4 and C3?
SLE most common
– Nephritic (Class III/IV): induction with steroids, and MMF or cyclophosphamide
– Nephrotic (Class V): ACEi/ARB for proteinuria and good BP control
IgA Nephropathy–> Associations? Prognosis? Treatment?
Associated with celiac, HIV, IBD, cirrhosis
-* Flares with infection
HSP: systemic IgA vasculitis with arthritis, purpura, GI symptoms; think children/young adults
– 50% progress to ESRD over 20-25yrs
– 50% enter remission (if proteinuria <1gram, rarely progress)
Treatment:
– ACEi or ARB if proteinuria >0.5-1g/day; titrate to proteinuria<1g/day
– Fish oil if persistent proteinuria >1g/day
– Consider steroids only for refractory proteinuria>1g despite above treatments
When would you consider full dose anticoagulation as prophylaxis for VTE in Membranous Nephropathy?
If albumin <25
These medications must be held if sick in CKD patients? Hint. Acronym is SADMANS
SADMANS medications – S-Sulfonylurea – A-ACEi – D-Diuretics – M-Metformin – A-ARBs – N-NSAIDS – S-SGLT2i
Biochemical targets for CKD mangement: K, HCO3, PO4 &Ca, PTH, Hg + Tsat + ferritin
– K <5
– HCO3 > 22
– PO4 and Ca toward normal range
– PTH target unknown for pre-dialysis CKD
– PTH target for dialysis patients is 2-9x ULN
– Hb 100-115, Tsat >30%, ferritin >500
Which patients with CKD should be on a statin?
- statin therapy for CV risk reduction in pts with CKD 3-5
- target treatment to LDL-C < 2 mmol/L
No evidence for patients on IHD!
What is CKD Mineral bone disease? How does it present and why do we care?
– Disorder of mineral metabolism manifested by: •Hyperphosphatemia • Hypocalcemia • Hypovitamin D • HyperPTH
Why does it matter? • Vascular calcification • Excess fracture risk • Excess risk of CV death • Excess risk of all-cause mortality
Routine BMD reasonable in patients with CKD3-5d if it will impact treatment decisions
Options for treatment if PTH is >9x ULN in dialysis patients? (remember target for non-dialysis patients is unknown)
What if PTH is >9x ULN?
– Calcitriol (1,25 Vit. D) but only if PO4 and Ca are not high
– Cinecalcet (a calcimimetic): activates Ca-sensing receptor to shut off PTH secretion
– Surgical parathyroidectomy in selected patients
How do you make the diagnosis of CKD in DM patients? ie. when should you screen and cutoffs for eGFR and ACR
Screen individuals w/ T1DM 5 years after diagnosis and T2DM at time of diagnosis then annually for CKD (ACR, serum Cr).
– eGFR<60 or ACR>2 in 2 of 3 samples over 3 months =CKD
Causes of elevated osmolar gap. Which cause a WAGMA in addition?
1,2,3 will cause AG as well as OG
High Osm Gap:
- Methanol
- Ethylene Glycol
- Paraldehyde
- Ethanol
- Isopropyl alcohol
- Mannitol
- Sorbitol
Urine AG formula
Urine AG= UNa+ + UK+ - UCl-
Type 1 RTA—>location, problem, K+, HCO3, Urine pH, associations
Location: Distal Problem: Decreased H+ secretion K+-VERY low HCO3- very low <10 Urin pH: >5.3 Association: CTD ie. Sjogren's
Can see stones!
Type 2 RTA—>location, problem, K+, HCO3, Urine pH, associations
Location: Proximal Problem: Decreased HCO3- reabsorption K+- low HCO3- 12-20 Urin pH: variable Association: Fanconi's, Myeloma
Can see Hypophosphatemia, phosphaturia, glucosuria, hypouricemia!
Type 4 RTA—> problem, K+, HCO3, Urine pH, associations
Problem: Hypoaldo state K+- HIGH! HCO3- >17 Urin pH: <5.3 Association: DM, HIV, Drugs (RASS blockers, aldo antagonists)
Calculation for volume of IVF to give in Hyponatremia?
Volume infusate to give = TBW x (desired Na – Serum Na)/ [Na] infusate
- Hypertonic saline 3%- 513mmol/L Na
- Normal Saline 0.9% - 154mmol/L Na
- Ringers Lactate- 130mmol/L Na
TBW= Total Body Water
For female- Wt (Kg) x 0.5
For Male- Wt (Kg) x 0.6
