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Renal Flashcards

1
Q

Top 5 kidney diseases leading to dialysis

A

1.Diabetes
2.GN
3.Vascular/HTN
4.ADPKD
5.Reflux

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2
Q

Benefit of balanced crystalloids in AKI

A

Less dialysis
Lower K
Less acidosis

also beneficial in transplant and in sepsis

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3
Q

Tumor lysis syndrome - electrolytes, risks, treatment

A

Rapid release of K, PO4, Ca, uric acid into the circulation

Risks: LDH, BM disease, high chemo radio sensitivity

Treatment
- IVT
- allopurinol - inhibits xanthine oxidase
- rasburicase - recombinant urate oxidase

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4
Q

IgA nephropathy treatment (4)

A
  1. Maximize RAS blockade + manage BP
  2. Address risk factors + lifestyle
  3. Consider SGLT2i
  4. Consider 6-months of steroids if at 90 days still 1g protein - avoid if high risk of SE: eGFR <30, diabetes, BMI >30, severe osteoporosis, cirrhosis, uncontrolled psych disorder, peptic ulcer, latent infection.

Offer clinical trials as no clear evidence

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5
Q

Management of GN complications - edema, hypertension, proteinuria, hyperkalemia, acidosis, hypercholesterolemia

A

Edema - loop diuretics + salt restriction

Hypertension - ACEi aiming <120/80

Proteinuria goal <1g/day

Hyperkalemia
- wasting diuretics: loop or thiazide
- potassium binders: petiromer, resonium

Metabolic acidosis HCO3<22 give sodium bicarbonate

Hypercholesterolemia - treat per guidelines - statin etc - decreased eGFR and albuminuria are independent CVD risk factors

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6
Q

GN not requiring biopsy - 2 definite plus 2 broad categories to consider with 7 conditions

A

Proteinuria in <12yo
Post-strept GN

Consider
- Membranous nephropathy with PLAR2
- PR3 or MPO positive vasculitis
- GBM with positive abs
- hereditary: Alport, fabry, familial fsgn
- SLE

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7
Q

When to consider (7) prophylactic anti coagulation in GN and agent of choice (3)

A

Albumin <20-25 AND one of:
1. Proteinuria >10g/day
2. BMI >35
3. Genetic
4. HF NYHA 3-4
5. Recent orthopedic or abdominal surgery
6. Prolonged immobilisation

Management
1. Warfarin
2. Heparin if hospital/ short term
3. Aspirin if albumin >32.
(DOAC do NOT have evidence and each have substantial renal clearance and albumin bound proportion which would impact dosing)

Membranous is high risk

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8
Q

Secondary causes of IgA nephropathy (4)

A
  1. Vasculitis
  2. Viral (HIV, Hepatitis)
  3. IBD and other autoimmune disease
  4. Cirrhosis
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9
Q

Elevated levels of soluble urokinase plasminogen activator receptor (suPAR) are associated
with which of the following renal conditions?
a. Membranous Glomerulonephritis
b. Focal Segmental Glomerulosclerosis (FSGS)
c. Membranoproliferative Glomerulonephritis (MPGN)
d. Minimal Change Disease
e. Anti-GBM Disease

A

Answer: B

Levels of suPAR have been found to be elevated in approximately 84% of adult patients with FSGS. suPAR has been shown to bind and activate podocyte β3 integrin, which leads to podocyte foot process effacement that is characteristic of proteinuric renal diseases.

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10
Q

All of the following situations may precipitate the formation and deposition of crystals in renal
structures leading to acute renal failure, EXCEPT:
a. IV acyclovir for severe herpes virus infections
b. Ethylene glycol toxicity or poisoning
c. Phosphate-containing laxatives in patients with CKD
d. Efavirenz used for HIV treatment
e. Tumour lysis syndrome as a result of cancer chemotherapy

A

Answer: D
Protease inhibitors Indinavir and Atazanavir used in HIV treatment can also lead to crystal nephropathies. However, Efavirenz has very minimal renal excretion in its active form. It is extensively metabolised in the liver by CYP450 3A4 and 2B6 systems and actually induces its own metabolism. Even when GFR is <10 mL/min or patients are on dialysis, it can be dosed as
in normal renal function.

In volume deplete patients, IV acyclovir is known to crystallize in red-green birefringent needle-
shape crystals that can block renal tubules.

Ethylene glycol toxicity and high doses of vitamin C
can both result in calcium oxalate crystal deposition in tubular cells and interstitium that can lead
to renal dysfunction.

Phosphate-containing laxatives may lead to acute phosphate nephropathy in patients with underlying renal impairment and hypovolemia.

In tumour lysis syndrome, uric acid crystallization in the tubules and collecting system may lead to a partial or complete obstruction of the collecting ducts, renal pelvis or ureter.

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11
Q

Minimal change disease (4)

A
  1. Nephrotic syndrome of childhood, but 10-20% adults
  2. Podocyte effacement on EM
  3. Adults relapse more
  4. Treat with prednisolone - 2nd line rituximab
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12
Q

Focal segmental GN (6)

A
  1. Nephrotic syndrome
  2. Hypertension +/- hematuria
  3. Glomerulosclerosis and hyalinosis effecting juxtamedullary nephrons first
  4. If persistent proteinuria then >50% will develop ESRF - fibrosis, hypertension, GFR also prognostic
  5. High recurrence in transplant (15-55%)
  6. Treat with prednisolone - 2nd line rituximab, cyclosporine
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13
Q

Primary membranous nephropathy (6)

A
  1. Nephrotic syndrome
  2. Thickened GBM with silver stain showing Ig deposits, spikes
  3. PLA2R - can guide investigation (secondary causes if negative) and treatment (based on titres and response)
  4. 25% ESRF in 10 years - nephrosis, HTN, Age, male, GFR
  5. Rituximab + steroids - 2nd line tacrolimus +/- MMF + pred
  6. Warfarin if albumin <20
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14
Q

IgA Nephropathy (6)

A
  1. Most COMMON nephritic syndrome
  2. Synpharyngitic
  3. Mesangial hypercellularity and matrix expansion. Interstitial damage and fibrosis with occasional crescents.
  4. 20% ESRF at 10 years - proteinuria, HTN, GFR, age, fibrosis
  5. ACEi + SGLT2i
  6. If minimal change overlap then prednisolone - otherwise risk outweigh benefit
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15
Q

Membranoproliferative GN (4) and treatment (4)

A
  1. Nephritic +/- nephrotic
  2. Secondary causes: hepatitis, Cryoglobulinemia, SLE, sjorgen’s etc (many)
  3. Membrane duplication = wire loops on silver stain, cellular proliferation, C3
  4. 40% ESRF at 10 years - nephrotic, GFR, interstitial disease

Treatment
5. If familial ACEi +/- SGLTi
6. If C3 - Eculizumab
7. If monoclonal treat for myeloma
8. If Hep C - sofosubivir/ velpatasavir

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16
Q

Rapidly progressive GN aka crescentic and subtypes (9)

A
  1. Renal failure
  2. Associated: hemoptysis, arthralgia/ myalgia, weight loss, lupus
  3. Crescents >50% glomeruli
  4. ANCA - most common, necrosis, eosinophils, pauci-immune
  5. GBM - linear IgG
  6. SLE - complement and granular antibody
  7. 50% ESRF - crescents, GFR
  8. Mortality due to pulmonary haemorrhage and sepsis
  9. Prednisolone pulse
  10. PO/IV cyclophosphamide or in ANCA use rituximab or in lupus use MMF
  11. Plasmapheresis for GBM, only in pulmonary haemorrhage for ANCA, NOT in SLE
17
Q

Which risk factor best predicts development of renal failure?
A. Age
B. Smoking
C. Hypertension
D. Obesity
E. GFR<90

A

E

  1. GFR
  2. Diabetes
  3. Age
  4. HTN
  5. Smoking
  6. BMI
18
Q

Most common cause of dialysis and most common GN leading to dialysis

A
  1. Diabetes
  2. GN - IgA most common
  3. HTN
  4. PKD
19
Q

In a patient requiring urgent dialysis which of the following parameters would favour continuous renal replacement therapy (CRRT) rather than intermittent haemodialysis (IHD)?

A. Active bleeding.
B. Coagulopathy.
C. Hyperkalaemia.
D. Hypotension.
E. Hypoxia.

A

D - CCRT is gentler

20
Q

67 y.o. diabetic on PD presents with abdominal pain, low grade fever and cloudy dialysate. She has mild generalised abdominal tenderness and guarding but does not appear particularly unwell. She is started on intra-peritoneal cephalexin. The next day, her dialysate culture grows:
Enterococci, E-coli and Klebsiella species.
The most appropriate management step is:

A. exploratory laparotomy.
B. add intraperitoneal Ampicillin.
C. removal of the Tenckhoff catheter.
D. intraperitoneal gentamicin.
E. change to intravenous antibiotics.

A

C

  • 50% Gram positives = SKIN
  • coagulase negative staph, staph aureus, enterococcus, streptococcus
  • 15% Gram negatives = GUT
  • 20% Culture negative = Don’t Know
  • 4% Polymicrobial infection = Laparotomy/Remove Tenckhoff
  • <2% Fungal infection = Panic and remove Tenckhoff

31% hospitalization i.e. most treated in the community

Treatment = gentamicin + cefazolin (replace with vancomycin if MRSA)

21
Q

With regards to haemodialysis patients, survival is improved by?

A. Tight BP control
B. Tight weight control
C. Dialysis dose
D. Dialysis duration
E. Tight cholesterol control

A

D - longer duration = better survival

urea reduction ratio also associated with survival

old age = risk factor

22
Q

Cardiovascular disease is the major cause of death in dialysis patients. Elevation of which of the following clinical parameters carries the highest mortality risk?

A. Serum phosphate.
B. Serum cholesterol.
C. Serum homocysteine.
D. Serum parathyroid hormone.
E. Blood pressure.

A

A - both PO4 and Ca are markers for mortality
- treatment with phosphate binders reduces mortality
- no association with PTH - though should treat with vitamin D +/- calcitriol

cholesterol has a paradoxical reverse association

BP in dialysis 120-170 equal risk - in practice aim <140

23
Q

Which of the following is most likely to increase serum phosphate in chronic renal failure?
A. Calcium trisilicate.
B. Calcitriol.
C. Cinacalcet.
D. Calcitonin.
E. Alendronate.

A

B. Calcitriol

Vitamin D leads to increased absorption of Ca and PO4 in the gut and reabsorption in the kidneys

24
Q

A 30-y.o woman presents with sustained HT (170/110 mmHg) on amlodipine monotherapy. Also on combined OCP. There is no radiofem delay or abdo bruit.
Investigation reveals the following:
Plasma renin activity <40 fmol/L/s [130-2350] Plasma aldosterone 320 pmol/L [80-1040] Serum potassium 3.9 mmol/L [3.5-5.5] Urinary metanephrines 1.3 μmol/24h [<1.5]
Which of the following secondary causes of HT is most likely?
A. ACTH-producing tumour.
B. OCP
C. Phaeochromocytoma
D. Primary hyperaldosteronism
E. Renal artery stenosis

A

D

25
Q

Which of the following carries the highest risk for mortality in dialysis patients:
A. Serum cholesterol 6.0 mmol/l
B. Blood pressure 110/75
C. Serum homocysteine 18 mmol/l (N < 13)
D. Body Mass Index (BMI) 36
E. Serum triglyceride 3.0 mmol/l

A

B

BMI and cholesterol have paradoxical relationships with CKD

C & E are not associated with mortality

26
Q

An otherwise stable dialysis patient has the following biochem:
Ca 2.50 mmol/l (N 2.1 – 2.6) Phos 2.1 mmol/l (N 0.8 – 1.5)
Albumin 44 gm/l (N 35 - 42) iPTH 35 pmol/l (N < 7)
The patient currently is prescribed CaCO3 600 mg i tds with meals. The most appropriate next step in management is:

A.Elective parathyroidectomy
B.Increasing CaCO3 to 2 tabs three times a day C.Adding Al(OH)3 1 tab three times per day D.Adopting a strict low phosphate diet
E.Adding calcitriol 0.25 ug daily

A

B
- phosphate is associated with mortality
- calcium acts as a phosphate binder

27
Q

A 60-year-old man with end-stage diabetic nephropathy received his first kidney transplant 6 months ago. Post transplantation, he had one episode of severe vascular rejection, which was treated with a course of anti-thymoglobulin (ATG). His graft function has been stabilised with serum creatinine of 190 umol/L (50-120 mol/L) while he is taking tacrolimus, mycophenolate and prednisolone. However, his renal function has progressively worsened in the past 2 weeks. His blood and urine BK virus polymerase chain reaction (PC) levels are very high. His preliminary kidney biopsy result reveals significant tubulitis, interstitial lymphocyte infiltration and intranuclear inclusion bodies were present. Which one of the following is NOT a treatment option?

A. Intravenous cidofovir to eradicate the BK virus
B. Intravenous methylprednisolone
C. Oral ciprofloxacin
D. Reduce tacrolimus and mycophenolate doses

A

B

The cause of rapid deterioration of graft function in this case is BK nephropathy (BKN). BK nephropathy is an important cause of premature graft failure. The risk factors associated with BKN include:
- Aggressive immunosuppressive treatment during the acute rejection, especially the usage of monoclonal antibodies such as anti-thymocyte globulin (ATG)
- Older recipient age
- Female donor
- HLA DR mismatching.
The management of BKN is challenging because no one therapeutic strategy is consistently effective. The reduction of overall immunosuppression is the cornerstone of treatment in BKN.
Cidofovir can competitively inhibit viral DNA synthesis. Cidofovir has been reported in small case series to have some benefit on BK, but its usage has been associated with substantial nephrotoxicity.
Leflunomide Is a pyrimidine synthesis inhibitor used in the treatment of rheumatoid arthritis. It is known to have both immunosuppressive and anti-viral properties. Single-centre reports of successful use of leflunomide for BKN have been published. There are no randomised, controlled trial data.
Ciprofloxacin has been used in the treatment of BKN. Quinolones may have anti-BK virus properties by inhibiting DNA topoisomerase activity and SV40 large T-antigen helicase. An observational study reported that use of a fluoroquinolone was associated with the prevention of BK viraemia after renal transplant.

28
Q

Hemodialysis complications (3 - not to due with fistula, graft, or catheter)

A
  1. Dialysis-disequilibrium syndrome
    * Cerebral edema due to osmotic effects of urea
    * Therefore start dialysis slowly
  2. Intradialytic hypotension & cramps
    * Pause or cease fluid removal
  3. Dialysis-related amyloidosis
    * Long-term (>5 years) accumulation of β2-microglobulin
    * Not seen much anymore since changing to high-flux dialyzers
29
Q

Renovascular hypertension - epidemiology, 2 common causes, degree of lesion required

A

15% will have renal artery stenosis on incidental imaging - however RAS accounts for 2-3% of HTN

Atherosclerosis - older, proximal, generally not amenable to intervention (except high risk) vs opposite in fibromuscular dysplasia

80% required to trigger renin increase
- in unilateral lesions one of the kidneys will work well and you don’t get fluid overload
- in bilateral lesions renin can be normal due to the volume expansion

30
Q

GN causes of low C4 (1), low C3 (3), both C3 and C4 (2)

A

Low C3 = cryoglobulinemia

Low C4
1. Atypical HUS
2. C3 glomerulopathy
3. Membranoproliferative GN

Both low
1. Post-infectious GN
2. Proliferative lupus

31
Q

IgA nephropathy associations (6)

A
  1. Cirrhosis - EtOH, Hep B, Hep C
  2. Celiac
  3. HIV
  4. Minimal change disease
  5. Membranous GN
  6. GPA
32
Q

ANCA Associated Vasculitis - genetics, likelihood of relapse, treatment

A

Family association - PR3 associated with HLA-DP

PR3 (GPA) - more likely to have relapsing disease

Treatment
- rituximab (superior to cyclophosphamide)
- avacopan = C5a receptor antagonist is non inferior to tapering prednisolone - can’t be used in liver disease

33
Q

Monoclonal Ig GN - histological subtypes

A

Mostly with associated underlying monoclonal gammopathy

Common = cast nephropathy, amyloidosis and Ig deposition disease

Uncommon = immunotactoid, proliferative, and light chain proximal tubulopathy

34
Q

Ig Deposition disease (2), immunotactoid, fibrillary - what gets deposited

A

Light chain = most common
Heavy chain = hypocomplementemia

Immunotactoid = IgG1

Fibrillary = IgG with C3

CLS (13 decks)

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