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RACP Written Exam 2015 > Renal > Flashcards

Renal Flashcards

0
Q

Regarding urine PH, which of the following is correct?
A. It is a useful indicator of the acid base balance of blood
B. It is determined by the concentration of ammonium
C. It is lower than 5.5 in RTA
D. It rises on a vegetarian diet
E. Would be above 7.0 after prolonged, severe vomiting

A

Answer is D.
Urine PH is affected by diet, with vegetarians having more ALKALINE urine compared to omnivores.

Animal proteins found in meat, eggs and cheese are often converted into acidic products such as Amino acids –> daily increase in the body’s acid content –> acid excreted in kidneys.

Calcium PO4 stones are more likely to form in alkaline urine with pH >6.0, therefore need to give dietary advice.

Other answers:
- Urine pH is determined by the concentration of H+ ions

  • bacterial infections often promote an ALKALINE urine due to the presence of bacterial enzymes converting Urea to ammonia
  • In RTA, unable to lower the pH to less than 5.5 in Type1 RTA
  • we do expect a pH of above 7.0 in severe vomiting to compensate for the loss of acid, but when there is hypovolaemia the retention of Na takes priority. Instead of HCO3 being excreted, it is reabsorbed in the proximal and distal nephron and this perpetuates the metabolic alkalosis until the fluid balance is restored.
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1
Q

What is the commonest cause of intrinsic AKI?

A

ATN

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2
Q

What is the benefit of measuring FGF-23 in dialysis patients?

A

FGF 23 in dialysis patients:

  • a good marker of mortality
  • the worse the GFR the higher the FGF 23
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3
Q

What is the most common cause of Acute Interstitial Nephritis?
How do you diagnose AIN?

A

PPI’s!

Diagnosis:
Eosinophilia on bloods
Urine may have eosinophilia and WCC casts

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4
Q

What is Hepatorenal Syndrome and what is the diagnostic criteria?

A

HRS is the development of renal failure with severe liver disease, in absence of any other renal pathology.

Diagnostic criteria (from BMJ):

  1. Cirrhosis with ascites
  2. Creat >133
  3. No improvement of serum creatinine despite 2 days of volume expansion and diuretic withdrawal
  4. Absence of shock
  5. No current / recent nephrotoxic drugs
  6. Absence of parenchymal kidney disease - need a normal renal US and No proteinuria / haematuria
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5
Q

What are the main drug causes of acute interstitial nephritis?

A

PPIs
Ciprifloxacin
NSAIDS
Beta lactam antibiotics

–> fever, rash, eosinophilia in urine/bloods, may have low grade proteinuria

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6
Q

What is the basic principle of management for PRIMARY Nephrotic Syndromes (Min change, Membranous, FSGS)?

A

1st line - Prednisone
2nd line - CTX
3rd line - CsA (but CsA nephrotoxic- tubulointerstitial nephritis)

The exception is Membranous Nephropathy where you give PRED and CTX TOGETHER for 6 months, ALTERNATING MONTHLY between the 2 drugs.
Also in Membranous, give WARFARIN if Albumin is low < 20 as there is a high risk of spontaneous DVT.

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7
Q

What is the management of Primary Membranous Nephropathy?

A

PREDNISONE and CTX TOGETHER for 6 months, ALTERNATING MONTHLY between the 2 drugs.

(steroid MONOTHERAPY does not work for Primary/Idiopathic Membranous Nephropathy)

WARFARIN if Albumin is low < 20 as there is a high risk of spontaneous DVT.

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8
Q

What is the antibody marker associated with Membranous Nephropathy?

A

PLA2R Antibody.

PLA2R Ab is present in 70% of Primary/Idiopathic MN.

It is NOT PRESENT in SECONDARY Membranous Nephropathy

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10
Q

What is the lab marker associated with FSGS?

A

SuPAR is a circulating Urokinase Receptor that is associated with FSGS.

(“Flash Gordon’S (FSGs) a “SuPAR-hero”)

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10
Q

What are the biopsy findings in Membranous Nephropathy?

A

LM/EM:

  • SPIKES on silver staining
  • Electron-dense deposits (= intramembranous deposits of Immunoglobulin)
  • thickened GBM
  • “granular” deposition

Late disease: interstitial fibrosis and less deposits

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11
Q

What are the secondary causes of Membranous Nephropathy?

A

*** HEP B!! - strongly associated!

Autoimmune diseases:

  • Diabetes (DIABETIC NEPHROPATHY MOST COMMON CAUSE)
  • SLE
  • RA

Drugs - ACEI, NSAIDS

Infections

Cancers - CLL

(Need to rule out these secondary causes in any patient with Membranous Nephropathy)

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12
Q

What is the prognosis of FSGS after treatment with steroids?

A

Depends if PRIMARY or SECONDARY FSGS.

PRIMARY FSGS:

  • good response to steroids
  • BUT in renal transplant, there is a VERY HIGH RISK OF DISEASE RECURRENCE (suspect if there is heavy proteinuria after transplant)

SECONDARY FSGS:

  • doesn’t respond to steroids or immunotherapy
  • but responds very well to kidney transplant

(Note the secondary causes of FSGS:
Ischaemic/ Renovascular,
reflux Nephropathy
HIV)

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13
Q

What are the biopsy findings in FSGS?

What part of the nephron is involved first?

A

LM/EM:

  • Sclerosis, FOCAL & SEGMENTAL (as the name implies)
  • Juxtaglomerular nephrons involved first
  • hyalinosis
  • interstitial fibrosis
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15
Q

What are the clinical characteristics of a patient presenting with Messngioproliferative Glomerulonephritis?

A

Typically a young male, HTN and nephrotic picture, LOW C3.
(Can look at MPGN as being “half nephrotic/half nephritic”)

MOST cases are due to SECONDARY CAUSES, eg.

  • SLE
  • Hep-C Associated Cryoglobulinaemia
  • -> Poor prognosis if nephrotic on presentation
  • -> ESRF in 40%
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15
Q

What is the treatment for Mesangioproliferative GN?

A

ASPIRIN +/- Dipyrimadole

(No benefit with Immunosuppression)

Treat underlying cause eg. SLE, HepC Cryoglobulinaemia etc

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16
Q

What are the biopsy findings in Mesangioproliferative GN?

A

(Note MPGN is also called Mesangio”CAPILLARY” GN)

LM/EM:

  • CAPILLARY BASEMENT MEMBRANE THICKENING
  • tubulointerstitial damage (looks like black dots on EM)
  • inflammatory infiltrate
  • cellular proliferation
  • Electron-dense deposits (= immunoglobulin)
  • If patient has LUPUS Nephritis = WIRE LOOPS = reduplication of membrane)
17
Q

What is the treatment for IgA Nephropathy?

A

ACEI (or ARB)

18
Q

What cell type is most involved in the pathogenesis of IgA Nephropathy?

A

Mesangial cells.

“Abberantly glycosylated IgA1” bind to IgG and form immune complexes which deposit in the MESANGIAL cells

  • -> hence on biopsy there is MESANGIAL CELL HYPERCELLULARITY
  • -> IgA positivity in Mesangial cells on Immunofluorescence confirms diagnosis of IgAN

also get interstitial damage and fibrosis.

19
Q

What kind of rash is associated with IgAN?

A

Leukocytoclastic Rash

= HSP!!

Henoch Schonlein Purpura is SYNONYMOUS with IgA nephropathy

20
Q

What is the strongest predictor for renal decline in ANY Glomerulonephritis?

A

Degree of PROTEINURIA
(Especially if not responding to treatment)

Proteinuria >1g is a predictor of ALL-CAUSE MORTALITY and Cardiovascular Events in renal disease.

21
Q

What are the clinical features of Goodpastures / Anti-GBM disease and how do you diagnose it?

A

Clinically - Haemoptysis and Haematuria (nephritic)

Pathophys- 
Type II Hypersensitivity reaction
Attacks the GBM antigen on the alveolar and glomerular basement membrane
Specifically attacks TYPE IV COLLAGEN
Results in Linear staining on IF.

Diagnosis:
IF: Linear stained IgG in GBM – “LINEAR DEPOSITS”
May also be pANCA positive.

22
Q

Patient presents with acute renal failure, haemoptysis, haematuria and proteinuria. Renal biopsy shows crescents. What is your management?

A

This is a medical emergency!
Diagnosis is RPGN (rapidly progressive GN, aka Cresenteric GN)

Suspect RPGN in any patient with Pulmonary Haemorrhage, renal failure and crescents.
CRESCENTS = bad = scarring/fibrosis
There is a risk of death. 50% develop ESRF.

MANAGEMENT:
1. Urgent biopsy & autoimmune screen
CLASSIFY INTO TYPES:
TYPE 1 RPGN: Anti-GBM / Goodpastures (pANCA) - COMMON
TYPE 2: SLE (“Wire Loops” on biopsy) or immune complex diseases
TYPE 3: (Pauci Immune) May be ANCA positive - (cANCA) WEGENERS (COMMON)

  1. IV Pulse Steroids (Methylpred) –> followed by high dose oral Pred
  2. CTX
  3. IVIG (but controversial) if Anti-GBM/Goodpastures or ANCA positive

(If SLE–> give MMF, IVIG and Rituximab)

NOTE - most common cause of RPGN is ANCA positive Vasculitis (Goodpastures or Wegeners)
DDx are Goodpastures, Wegeners, MPA, SLE

24
Q

What are the different types of Lupus Nephritis? (5)

A

Important to differentiate the types of Lupus Nephritis because the treatment differs for Class IV.

Class IV - treat with MMF
All others - treat with AZA

Class I - normal or minimal kidney disease
Class II - Mesangial deposits, Mesangial proliferation
Class III - FOCAL proliferative GN (less than 50% glomeruli affected)
Class IV - DIFFUSE proliferative GN (more than 50% glom affected)
Class V - Membranous GN

25
Q

What is Eculizumab? MCQ

A

Used in HUS
Eculizumab blocks COMPLEMENT C5
Treatment is for 26 weeks (6 months)

25
Q 
Tumour Lysis Syndrome causes Acute Tubular Necrosis.
What is the
1. Prevention
and
2. Treatment
of TLS?
A

Important to know physiology:
Xanthine –> converted to Uric acid (via XO). Uric acid forms urate crystals that block up the tubules. Uric acid –> acidic pH.

Uric acid –> metabolised to Allantoic acid (via Urate Oxidase)

Prevention:

  1. Hydration
  2. Allopurinol
  3. Urinary alkalinisation

Management:

  1. Rasburicase (potentiates the action of Urate Oxidase)
  2. Hydration
26
Q

What are the causes and pathogenesis of HUS-TTP?

A 
Causes:
Surgery
Transplant
Pre-Eclampsia / Pregnancy
Malignant HTN
Drugs
Cancer
Infection
Anti phospholipid syndrome

Pathogenesis involves activation of the ALTERNATE Complement pathway - C3 convertase –> MAC attack
(Hence Eculizumab/C5 blockade used as treatment)

27
Q

How do you diagnose Hepatorenal Syndrome?

A

Clinically -
Renal failure with severe liver disease (cirrhosis, ascites, jaundice) in the absence of any other renal pathology.

  • Na retention in PROXIMAL tubule *
    Often hypotensive and low urine output
DIAGNOSIS:
Urine Na <10
Renal impairment
Bland urinary sediment - little/no urine protein or blood
No renal obstruction on US
Failure to improve with volume expansion
28
Q

What is the management for Hepatorenal Syndrome?

A

Volume expansion with:

  • ** TERLIPRESSIN (ADH/Vasopressin analogue) PLUS ALBUMIN **
  • IV fluids
  • Dialysis
  • LIVER TRANSPLANT is the only definitive management
29
Q

What are the types of Acute rejection in renal transplant medicine, and how do you treat them?

A

Acute Rejection occurs in 15-25% of individuals
Occurs early in first 3 months
TREATABLE!

2 TYPES OF ACUTE REJECTION:

  1. T-Cell mediated –> treat with STEROIDS
  2. Donor-specific Antibody mediated –> treat with PLASMAPHERESIS or MMF
30
Q

Transplant Rejection Prophylaxis.

What are the side effects of the Calcineurin Inhibitors?

A

COMMON side effects:

  • Nephrotoxic –> Chronic Allograft Nephropathy
  • ** HUS!!! **
  • Thrombocytopaenia
  • Hepatotoxic
  • ** Avascular Necrosis / Bone pain
CYCLOSPORINE (CSA) side effects:
- HTN
- Lipids
- Gingival hyperplasia
- Hirsutism
(Basically CSA makes you fat and ugly!)

TACROLIMUS side effects:
- Diabetes
- Peripheral neuropathy
(“Tic TACs give you Diabetes”)

31
Q

Induction therapy is used for high risk renal transplants to minimise Acute Rejection. What are the main Induction agents used?

A

Main aim is to target T cells to prevent Tcell-mediated acute rejection.

Induction agents:
ANTI-THYMOCYTE GLOBULIN (THYMOGLOBULIN)
- kills T cells. Causes T Cell Lysis (takes 6 months for T cells to recover)
- targets are T cells and ICAM
- rabbit polyclonal Ab
- S/E: CANCER, infection, thrombocytopaenia, LVF, meningitis

BASILIXIMAB

  • IL-2 Receptor blocker –> inactivates T cells
  • not as good as thymoglobulin
  • used in acute rejection, not chronic rejection
32
Q

What is the target Ferritin level in dialysis patients?

A

Target Ferritin is > 200 in Dialysis patients.

Aim for higher ferritin as there is reduced ability to access Fe stores in ESRF and HD filters out more Fe.

** replace Fe before giving EPO

** Ferritin is an acute phase reactant, hence in inflammation (High Fe) –> there may be EPO resistance and anaemia

33
Q

Immunosuppression in Renal Transplant.

What are the agents used for transplant rejection prophylaxis and what are their mechanisms of action?

A

Principles of Immunosuppresion:

  • Use multiple agents in combination, to minimise toxicity
  • Use INDUCTION therapy to minimise acute rejection
  • Use Valaciclovir prophylaxis against CMV, and monitor for steroid-induced OP
  1. INDUCTION AGENTS
    - Thymoglobulin (Antithymocyte Globulin) –> T cell LYSIS
    - Basiliximab (IL-2R Ab)
    - ——————————
  2. STEROIDS for 3 months, then taper
    - ——————————
  3. SIGNAL 1 INHIBITION = i.e. CALCINEURIN INHIBITORS (CSA or TAC) for 3 months = blocks IL2

CSA:
–> binds CYCLOphylin which forms a complex with Calcinuerin and prevents Calcinuerin from upregulating IL2/other cytokines that activate T cells

TAC:
(“Stale TACo’s are used “For Killing Bad People!” / FKBP”)
–> binds FKBP and forms a complex that inhibits Calcineurin, thereby inhibiting T cell activation

  1. ANTIPROLIFERATIVES = Block downstream T cell proliferation
    - AZA (Thiopurine. Purine antimetabolite / blocks purine synthesis and DNA synthesis)
  • ## MYCOPHENOLATE (blocks purine synthesis / G1 arrest. INHIBITS INOSINE MONOPHOSPHATE DEHYDROGENASE. Action against lymphocytes)
    1. SIGNAL 3 BLOCKADE = mTOR INHIBITORS = block IL2
  • SIROLIMUS, Everolimus
    (“SIRIUS Black from Harry Potter is known “For Killing Bad People”)
    –> binds FKBP –> blocks IL-2 signalling by blocking the downstream molecule mTOR –> G1 arrest –> inhibits DNA synthesis
    –> S/E: INTERSTITIAL PNEUMONITIS in 23%, Proteinuria, Lipids +++
    –> Not Nephrotoxic and does not cause CAN :)
    ——–
    MAINTENANCE THERAPY:
    CsA and MMF
34
Q

What is the target Hb level in Dialysis patients?

A

Hb should be 110-115.

Increased mortality risk if:
Too high >130 (clots off fistula –> increases BP)
Too low < 100 (anaemia!)

EPO can be started when Hb <100-110

35
Q

What is the target BP level in Dialysis patients?

A

KEEP BP HIGHER, aim for BP 140/90.

Do NOT lower BP to systolic 120! Increased mortality risk if SBP <120.

Try to control BP with fluid removal alone.

36
Q

What is the role of statins in Dialysis patients?

A

Statins NOT BENEFICIAL in Dialysis patients.
Plaques tend to be CALCIFIC (Ca++ and PO4–)
rather than Lipid-rich

37
Q

Define “Resistant HTN”.

A

Resistant HTN = Uncontrolled BP on THREE DIFFERENT AGENTS at max doses, with one of the agents being a DIURETIC

38
Q

What is the management of Renovascular HTN / Renal artery Stenosis?

A

MEDICAL MANAGEMENT ONLY!

First line is ACEI/ARB.

(There is NO BENEFIT in Stenting, Renal Denervation, or even performing a CT renal angiogram as it overestimates RAS and it won’t change management as there is no benefit to surgery anyway)

39
Q

Renal Tubular Acidosis.

How do you differentiate the different types of RTA?

A

RTA is a NAGMA which usually presents with Hyperchloraemia.

3 clinically relevant RTAs :

Type 1 RTA: (the most acidotic!)
- DISTAL
- Due to IMPAIRED ACID/H+ EXCRETION in the distal tubule
- Bloods: 
HCO3 LOW
K usually LOW
May have high Calcium
- Urine pH: > 5.5 (BASIC)
- ** Associated with SJOGRENS, RA, **RENAL CALCULI**

Type 4 RTA: (most common)
- DISTAL
- Due to IMPAIRED CATION EXCHANGE in distal tubule, associated with ALDOSTERONE DEFICIENCY/UNRESPONSIVENESS
(results in More K reabsorbed –> high K –> reduced ammonia excretion & therefore –> Acidosis)
- Bloods:
HYPERKALAEMIA
HCO3 HIGH
Urine pH LESS THAN 5.5 (ACIDIC URINE)
- Examples: DM Nephropathy, chronic interstitial nephritis, ANY RAAS impairment, NSAIDS, Heparin, Critical illness, Adrenal insufficiency

Type 2 is rare

  • PROXIMAL tubule
  • Impaired HCO3 reabsorption –> BASIC Urine pH >7.0 if plasma HCO3 is normal (Urine pH <5.5 if plasma HCO3 is depleted and there are ongoing renal losses)
  • eg. Fanconi, Myeloma light chain Nephropathy, antivirals, acetazolamide
40
Q

What investigations would give you a diagnosis of HUS-TTP?

A

Findings in both TTP and HUS:
Renal biopsy = Thrombotic microangiopathy
Platelets usually LOW, less than 150
Haemolysis - low Hapto, high LDH but Coombs neg
SCHISTOCYTES on film (= RBC fragments)

TTP
FATRN clinically - Fever, Anaemia, Thrombocyto, Renal Imp, Neuro Sx
LOW ADAMTS13 to less than 5% of normal range

HUS—
SHIGATOXINogenic E.Coli (STEC) or Shigella
Diarrhoea clinically
Pathogenesis activates COMPLEMENT pathway, C3 –> MAC attack
(** hence the use of ECULIZUMAB a complement blocker, for 26/52 for HUS)

RACP Written Exam 2015 (14 decks)

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