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Bpt > Renal > Flashcards

Renal Flashcards

1
Q

Clinical Triad:
• A precipitating event (such as aortic or coronary angiography)
• Subacute or acute kidney injury
• Typical skin findings, such as blue toe syndrome and/or livedo reticularis

A

Iatrogenic/cholesterol emboli

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2
Q

Role of ADH in Kidneys

A

Inserted aquaporin 2 channels in collecting duct in response to water deprivation leading to increased water absorption and thus more concentrated urine

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3
Q

ATN Definition

A

Reversible or irreversible type of renal failure caused by ischaemic or toxic injury to the renal tubular epithelial cells. The injury results in cell death or detachment from basement membrane causing tubular dysfunction.

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4
Q

Aminoglycoside Nephrotoxicity

A
  • Manifests after 5-7 days of therapy
  • Causes ATN, polyuria due to distal tubule damage, and decrease in most electrolytes due to PCT impairment
  • Major risk factor is prolonged use (even if perfect control of plasma concentration)
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5
Q

ATN Findings

A

Muddy Brown Casts

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6
Q

Type of ATN in patients with rhabdo and haemolysis

-Features: red/brown urine, granular casts, oliguria/anuria

A

Acute pigment cast nephropathy

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7
Q

Drug causes of AIN

A

●NSAIDs
●Penicillins and cephalosporins
●Rifampin
●Antimicrobial sulfonamides, including trimethoprim-sulfamethoxazole
●Ciprofloxacin and, perhaps to a lesser degree, other quinolones
●Diuretics, including loop diuretics such as furosemide and bumetanide, and thiazide-type diuretics
●Cimetidine (only rare cases have been described with other H-2 blockers such as ranitidine)
●Allopurinol
●PPIs such as omeprazole and lansoprazole
●Indinavir
●5-aminosalicylates (eg, mesalamine)

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8
Q

Causes of Drug induced TMA

A

Quinine, Type 1 interferon, Cancer therapies, Calcineurin inhibitors

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9
Q

IgA Renal Biopsy Findings

A

Pathognomonic finding is observed on immunofluorescence microscopy, which demonstrates dominant or codominant mesangial deposits of IgA, either alone, with IgG, with IgM, or with both IgG and IgM.

Poor Progonostic features:

  • Subendothelial capillary wall IgA deposits
  • IgG codeposition
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10
Q

Synpharyngitic haematuria - IgA

A
  • 40-50% present of patients
  • One or recurrent episodes of gross (visible) hematuria, often accompanying an upper respiratory infection
  • Most patients have only a few episodes of gross hematuria, and episodes usually recur for a few years at most
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11
Q

Microcytic Haematuria - IgA

A

 30-40% of patients with IgA nephropathy
 Usually associated with mild proteinuria
 Disease of uncertain duration for these patients
 Gross hematuria will eventually occur in 20 to 25 percent

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12
Q

IgA Nephrotic syndrome/RPGN

A

 Less than 10% of patients
 Oedema, HTN, renal insufficiency, and haematuria
 May rarely present with malignant HTN

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13
Q

IgA nephropathy Associations

A 
o	Cirrhosis/CLD
o	Coeliac Disease
o	HIV
o	Granulomatosis with polyangiitis
o	Minimal change disease and membranous nephropathy
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14
Q

Mx of IgA nephropathy

A
  1. BP control w/ ACE/ARB
  2. Statin if LDL raised to lower CVD risk
  3. Immunosuppression in severe cases
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15
Q

Indications for Immunosuppression in IgA nephropathy

A

Immunosuppressive therapy is indicated if there is haematuria plus one of the following
• Progressive decline in GFR
• Persistent proteinuria >1g/day on maximal ACE or ARB for 3-6 months
• Morphologic evidence of active disease on kidney biopsy (proliferative or necrotising glomerular changes)

usually corticosteroid +/- cyclophosphamide/azathioprine

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16
Q

Clinical predictors of poor prognosis in IgA nephropathy

A

 Higher serum creatinine at diagnosis
 HTN - BP >140/90 at disease discovery
 Protein Excretion > 1g/day - the incidence of dialysis and death was significantly higher

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17
Q

3 CArdinal Features of Scleroderma Renal Crisis

A

o Abrupt onset of moderate to severe hypertension
o AKI
o Normal urinalysis

May also present with APO/CCF

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18
Q

Risk Factors for SRC

A

o Diffuse Skin involvement (Most important risk factor, especially if it is rapidly progressive)
o Glucocorticoid use (>15 mg/day)
o Anti RNA Polymerase III

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19
Q

Renal Bx for SRC

A

o Characteristic finding on histopathology is intimal proliferation and thickening that leads to narrowing and obliteration of the vascular lumen, with concentric “onion-skin” hypertrophy

Renal Bx does not diagnose SRC deut o similarities with TMAs

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20
Q

Treatment of SRC

A
  1. Captopril - improves renal function and survival; second line add on CCB
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21
Q

Prognosis of SRC

A

20-50% of patients will require dialysis temporarily.
Most will be able to regain renal function slowly up to 18 months after starting HDx, Thus transplantation delayed for at least 6 months post starting HDx

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22
Q

Infections/AI Diseases causing AIN

A 
Legionella
Leptospira
CMV
Streptococcus
Mycobacterium tuberculosis
Corynebacterium diphtheriae
EBV
Yersinia
Polyomavirus
Enterococcus
Escherichia coli
Adenovirus
Candida
HIV

SLE
Sarcoidosis
Sjogrens
IgG4 Disease

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23
Q

AIN Investigations

A

WCC casts - most specific

o Increased Creatinine
o Eosinophilia (25-35% of cases)
o Eosinophiluria - >1% of urinary WCCs (not specific for AIN)
o Urine sediment: WDD, RBC, white cell casts
o Variable proteinuria from non or minimal to >1gram/day

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24
Q

Indications for Renal Bx for AIN

A
  • Patients who have a characteristic urinalysis for AIN but are not being treated with a drug known to cause AIN.
  • Patients who are being treated with a drug known to cause AIN but do not have a characteristic urinalysis.
  • Patients who are being considered for treatment with glucocorticoids for AIN (usually drug induced).
  • Patients with putative drug-related AIN who are not treated with glucocorticoids initially and do not have a recovery following cessation of drug therapy
  • Patients who present with advanced renal failure (relatively recent onset <3 months)
  • Patients with any features (such as high-grade proteinuria) that cause the diagnosis of AIN to be uncertain.
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25
Q

AIN Renal Bx findings

A
  • Interstitial oedema and a marked interstitial infiltrate consisting primarily of T lymphocytes and monocytes
  • Eosinophils, plasma cells, and neutrophils also may be found
  • The classic lesion of “tubulitis” is found when inflammatory cells invade the tubular basement membrane
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26
Q

Types of GN associated with RA

A

Direct effect:

  • FSGS
  • mesangioproliferative
  • membranous
  • Rheumatoid Vasculitis

Drug Toxicity
Amyloidosis (AA) in longstanding poorly controlled, seropositive RA

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27
Q

Clinical Features of Amyloidosis

A
  • vary depending on location of disease and type of amyloid
  • waxy skin and easy bruising
  • enlarged muscles (eg, tongue, deltoids)
  • symptoms and signs of heart failure
  • cardiac conduction abnormalities
  • hepatomegaly
  • evidence of heavy proteinuria or the nephrotic syndrome
  • peripheral and/or autonomic neuropathy
  • impaired coagulation
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28
Q

EPO Stimulus

A

• Major stimulus for EPO production is decreased oxygen delivery due to reduced red blood cell mass (anaemia) or decreased O2 saturation of red cell haemoglobin (hypoxia)

  • The Epo promoter is suppressed by GATA-2 in normoxia. GATA-2 levels decrease in hypoxia
  • More importantly, the Epo enhancer is activated by hypoxia-inducible transcription factors (HIFs).
  • EPO targets CFU-E, proerythroblasts, and basophilic erythroblast portion of Hb production
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29
Q

HUS Definition

A

the simultaneous occurrence of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury

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30
Q

Causes of Atypical HUS

A

o Complement gene mutations
o Antibodies to complement factor H
o Diacylglycerol kinase epsilon gene mutations
o Inborn error of cobalamin C metabolism

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31
Q

Causes of typical HUS

A

o Infection:
 STEC
 Streptococcus pneumoniae
 Human immunodeficiency viral infection
o Drug toxicity, particularly in patients with cancer or solid organ transplant recipients
o Rare occurrences in pregnant patients or in those with autoimmune disorders (eg, systemic lupus erythematous)

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32
Q

HSP Tetrad

A

o Palpable purpura in patients with neither thrombocytopenia nor coagulopathy
o Arthritis/arthralgia
o Abdominal pain
o Renal disease

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33
Q

HSP Bx Findings

A

characteristic finding of IgAV (HSP) is leukocytoclastic vasculitis accompanied by IgA immune complexes within affected organs

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34
Q

Myogenic reflex

A
  • A first line defense against fluctuations in renal blood flow
  • Acute changes in renal perfusion pressure evoke reflex constriction or dilatation of the afferent arteriole in response to increased or decreased pressure, respectively
  • This phenomenon helps protect the glomerular capillary from sudden changes in systolic pressure
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35
Q

Tubuloglomerular Feedback (TGF)

A
  • TGF changes the rate of filtration and tubular flow by reflex vasoconstriction dilatation of the afferent arteriole.
  • TGF is mediated by specialized cells in the thick ascending limb of the loop of Henle called the macula densa that act as sensors of solute concentration and tubular fluid flow rate
  • With high tubular flow rates, a proxy for an inappropriately high filtration rate, there is increased solute delivery to the macula densa that evokes vasconstriction of the afferent arteriole causing GFR to return to normal
  • One component of the soluble signal from the macula densa is ATP released by the cells during increased NaCl reabsorption. ATP is metabolized in the extracellular space to generate adenosine, a potent vasoconstrictor of the afferent arteriole.
  • During conditions associated with a fall in filtration rate, reduced solute delivery to the macula densa attenuates TGF, allowing afferent arteriolar dilatation and restoring GFR to normal levels. Angiotensin II and reactive oxygen species enhance, while NO blunts TGF
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36
Q

Angiotensin II effect on Renal Blood Flow

A
  • During states of reduced renal blood flow, renin is released from granular cells within the wall of the afferent arteriole near the macula densa in a region called the juxtaglomerular apparatus.
  • Renin, a proteolytic enzyme, catalyzes the conversion of angiotensin to angiotensin I, which is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE)
  • Angiotensin evokes vasconstriction of the efferent arteriole, and the resulting increased glomerular hydrostatic pressure elevates GFR to normal levels
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37
Q

Drugs that elevate the Serum Creatinine

A

Trimethoprim, cemetidine, Dolutegravir, cobicstat, PARP inhibitors, TKIs

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38
Q

Pathophysiology of diabetic nephropathy

A
  1. Hyperfiltration assocaited with increased renal size
  2. Microalbuminuria (30-300mg/day or ACR 3.5-35)
  3. Macroalbuminuria (>300 mg/day or ACR >35)
  4. ESRF
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39
Q

Role of Bicarb Therapy in CKD

A

Metabolic acidosis in non dialysis dependent CKD associated with higher mortality and low bicarb associated with higher risk of progressive renal function loss.

  • Bicarb supps slow progression of CKD by reducing acidosis and decreasing H+ reabsorption
  • Bicarb also improves bone health, protein production, nutritional status, reduces lipids, and improves insulin sensitivity
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40
Q

CVS risk in CKD

A

An increased risk of death and cardiovascular mortality as GFR falls below 60ml/min/1.73m2 or when albumin is detected on urinalysis

Modifications:
• Smoking cessation
• Exercise
• Weight reduction to optimal targets
• Lipid modification recognising that the risk reduction associated with statin therapy in adults with CKD is relatively constant across a broad range of baseline low-density lipoprotein cholesterol (LCL-C) levels
• Optimal diabetes control HbA1c <7% (55mmol/mol)
• Optimal BP control to <140/90mmHg or 130/80 mmHg in those with CKD and depending on the degree of proteinuria **
• Aspirin is indicated for secondary prevention but not primary prevention.

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41
Q

MOA and Contraindications for EPO

A

MoA: Recombinant glycoproteins that bind to erythropoietin receptors on erythroid progenitor cells. Stimulate erythropoiesis, increasing reticulocyte count, haematocrit and haemoglobin concentration.

Contraindicated: uncontrolled hypertension

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42
Q

Side effects of EPO

A

Common (>1%):
Hypertension (esp with rapid haemoglobin rise), headache, flu-like symptoms, bone pain, myalgia, fever, rash, peripheral oedema

Rare (<1%): 
Hypertensive encephalopathy (inc seizures), allergy (inc. angioedema and anaphylaxis), pure red cell aplasia (more likely with subcut route)
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43
Q

Pure red cell aplasia

A

Complication of EPO

  • Autoantibodies in the serum of these patients neutralized both recombinant human erythropoietin and endogenous erythropoietin
  • Dependent on Transfusions and need immunosuppression
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44
Q

Contraindications to PD

A

1) Peritoneal scarring
2) Anuria or large patient size
3) Active inflammatory process or cancer
4) Surgical ostomies
5) Large abdominal wall hernia
6) Ventriculoperitoneal shunts

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45
Q

Common Cancers in Renal Transplant

A
  1. Skin cancers (basal cell and squamous cell carcinomas) – Human papilloma virus HPV
    - BY FAR THE HIGHEST IS SCC
  2. Lymphoproliferative disorders – likely due to Epstein-Barr virus
  3. Kaposi’s sarcoma – Human herpes virus 8 HHV-8
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46
Q

Evidence of statins in CKD

A

statin therapy is associated with reduced cardiovascular risk and total mortality but with no significant effect on CKD progression

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47
Q

Hba1c target in CKD

A

7%, below this is associated with increased risk of hypos and possibly death

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48
Q

Metformin Dosing in CKD

A

CrCl > 90 (max 3g daily)
CrCl 60-90 (max 2g daily)
CrCl 60-30 (max 1g daily
CrCl <30 → contraindicated

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49
Q

Indications for RRT in AKI

A

AEIOU = Indications for Urgent Dialysis in Acute Kidney Injury

A Acidosis Metabolic acidosis with a pH <7.1

E Electrolytes Refractory hyperkalemia (K>6.5 mEq/L) or rapidly rising potassium levels

I Intoxications Some toxins can be removed with dialysis SLIME (salicylates, lithium, isopropanol, methanol, ethylene glycol)

O Overload Volume overload refractory to diuresis

U Uraemia Elevated BUN + signs/symptoms of uraemia pericarditis, neuropathy, uremic bleeding, uremic encephalopathy

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50
Q

FGF 23 function

A

FGF-23 is secreted by bone osteocytes and osteoblasts in response to Hyperphosphataemia.

  • Decreases serum phosphate by reducing reabsorption in renal tubules and decreases Vit D 1a hydroxylase expression
  • Klotho is co factor needed for expression
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51
Q

Pathophysiology of oedema in nephrotic syndrome

A

• Primary sodium retention that is directly induced by the renal disease (overfill hypothesis)
i.e. increased sodium reabsorption in the collecting tubules, which is also the site of action of atrial natriuretic peptide (ANP)
• Secondary sodium retention in which the low plasma oncotic pressure due to hypoalbuminemia promotes the movement of fluid from the vascular space into the interstitium, leading to underfilling of the vasculature and activation of the renin-angiotensin-aldosterone system (underfill hypothesis)

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52
Q

Management of oedema in nephrotic syndrome

A
  1. Diuretic
  2. Sodium restriction 2g/day

Non responders:

  1. Thiazide to block sodium resorption
  2. Acetazolamide
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53
Q

Reason for higher Frusemide dose in CKD

A

• All the commonly used diuretics are highly protein-bound. This limits the diuretic to the vascular space, thereby maximizing its rate of delivery to the kidney. The degree of protein-binding is reduced with hypoalbuminemia, resulting in a larger extravascular space of distribution and a slower rate of delivery to the kidney

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54
Q

Relationship between retinopathy and diabetic nephropathy

A

o RETINOPATHY is almost universal in all patients with T1DM and DN:
o Less concurrence with T2DM (50-75%)
o K/DOQI Guidelines: If retinopathy absent, should suspect other causes of CKD
o Converse is not true ie. Retinopathy can occur without DN

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55
Q

Screening Timeline for DN

A

T1DM - at age 9 with 2 year duration of diabetes
T2DM: at diagnosis

Then yearly for both

If microalbuminuria -confirm with 2 out of 3 abnormal tests over 2-12 weeks

If macroalbuminuria: Confirm with 24 hour protein = >0.5g/24 hours

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56
Q

Features suggesting alternative cause of CKD in diabetic patients

A

• Onset of proteinuria <5 years after onset of T1DM
-Same applies for T2DM but time of onset is often difficult to ascertain as Dx is often delayed
• Acute onset of kidney injury or nephrotic syndrome (diabetic nephropathy is usually slowly progressive)
• Presence of active urinary sediment containing red cells or cellular casts
• In T1DM, absence of diabetic retinopathy or neuropathy
• Signs or symptoms of another systemic disease
• Significant reduction in eGFR (<30%) after introduction of ACE or ARB
-More consistent with RAS or arteriosclerotic renal disease

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57
Q

Hb Target in CKD

A

100-110

  • Trial iron first then EPO
  • Increased mortality associated with higher Hb if using EPO
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58
Q

Target phosphate levels in CKD

A
  • Non-dialysis patients - within normal range

* Dialysis patients – 1.12-1.78mmol/L

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59
Q

Phosphate binders MOA and benefit in CKD

A
  • Block absorption of phosphate from the small intestine, therefore must be taken with meals
  • Non-calcium containing phosphate binders have been shown to decrease mortality in dialysis patients
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60
Q

Mx of Refractory hyperphosphatemia

A

• Calcimimetics, e.g., cinacalcet

  • Increase sensitivity of calcium-sensing receptor in the parathyroid glands to calcium
  • Reduce levels of PTH, calcium and phosphate

• Parathyroidectomy
-Effectively treats hyperparathyroidism related hypercalcaemia, hyperphosphaaemia, bone pain, pruritis and myopathy

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61
Q

Two main causes of Renal Artery stenosis

A
  • Atherosclerotic disease
  • -Usually proximal renal artery
  • Fibromuscular dysplasia
  • -Typically women 30-50 yo
  • -USually mid to distal renal artery and characteristic string of beads on imaging
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62
Q

Affect on BP, renin, and volume state in unilateral RAS

A

Increased BP
Increased Renin
Normal Volume state

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63
Q

Affect on BP, renin, and volume state in bialteral RAS

A

Increased BP
Normal Renin
Increased volume state (due to loss of pressure natuersis)

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64
Q

Define the Pickering Syndrome

A

Flash APO secondary to bilateral RAS in the setting of normal LVEF

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65
Q

Testing for Renal Artery Stenosis

A

Gold Standard - Conventional Angiography

First test:
Doppler USS
–95% NPV (look at peak systolic velocity)

Resistive index:
-Represents amount of small vessel disease (High if >0.70)

CTA and MRA:
-Concern for contrast, but can be used

ACEi Scitinigraphy
- Administration of ACE will cause reduction in efferent tone so in the setting of a fixed lesion in the afferent vessel egfr will drop

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66
Q

Mx of RAS

A

BP - RAAS blockade, CCB, thiazide

CVS risk factors

Stenting for FMD only has shown benefit thus far only low quality evidence for severe atherosclerotic disease. No benefit in mild-mod atherosclerotic disease

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67
Q

Renal effects of NSAIDs

A

NSAIDS lead to PG#2 and PGI2 inhibition

  • Leads to Sodium retention (oedema, BP, weight), hyperkalemia, and ARF
  • Also inhibit dilation of afferent arteriole, so when used with ACEi (which dilate efferent arteriole) you drop egfr
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68
Q

Effect of angiotensin on the kidney

A

Maintains efferent arteriolar tone
Relaxation of efferent arteriole results in reduced intraglomerular pressure
So ACE and AII reduce gfr as part of their mechanism of action

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69
Q

SE of VEGF inhibitors on kidneys

A

GN type picture similar to MCD, podacyte effacement

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70
Q

S-FLT-1

A

Circulating VEGF receptor

High levels may be a marker for pre-eclampsia

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71
Q

Prevention of pre-eclampsia

A

150 mg aspirin in early pregnancy

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72
Q

Mx of pre-eclampsia

A

Delivery if >37 weeks (if severe deliver >32 weeks)
Labetalol QID
MgSO4 to prevent seizures

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73
Q

Medullary Sponge Kidney

A

MAlformation of the terminal collecting ducts

  • Results in microscopic and macroscopic Medullary cysts
  • Bialteral
  • Benign but assocaited with stones and UTIs
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74
Q

Medullary Cystic Kidney

A

No renal cysts
Predominantly a tubulo-interstitial disorder
-Progresses to ESRD

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75
Q

Acquired Cystic disease (in renal failure/impairment)

A

Multiple and bilateral renal cysts

Distnguish from ADPCKD:
-No FHx, small to normal sized kidneys, smooth contour

Associated wit hRCC

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76
Q

Most common genetic cause of CKD

A

ADPCKD

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77
Q

Genes and their presentation in ADPCKD

A

PKD-1

  • More rapid deteriroation in renal function, more cysts
  • Median age of ESRD 54

PKD-2

  • More indolent decline in renal function
  • Median age of ESRD 74

PAthophysiology:
Polycystin mutation and these regulate tubular and vascular development in multiple organs

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78
Q

Tolvaptan Indication, MOA, SE, Evidence

A

Vasopressin receptor antagonist

Indication: ADPCKD

MOA: Suppression of vasopressin release reduces second messenger systems (cAMP) identifed as promoters of kidney cyst cell proliferation and luminal fluid secretion

Evidence: Decrease in cyst size, reduction in rate to ESRD, slows egfr decline

SE:
LFT derrangement
Polyuria/polydipsia (Avoid with diuretics and w/h when unwell)
Hyperuricemia

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79
Q

Criteria for diagnosis of AKI

A

-Increase in Serum Cr >26.5 micromol/l within 48 hours

OR

-Increase in Serum Cr > 1.5 times baseline within the last 7 days

OR

UO < 0.5 ml/kg/hr for 6 hours

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80
Q

Risk Factors for AKI

A 
Main: Age
Proteinuria
CKD
Other Comorbidities
Nephrotoxic meds
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81
Q

Significance of AKI

A

Increased rates of mortality and CKD down the track

Worse the AKI the higher the mortality

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82
Q

Which part of the kidney is most sensitive to hypoprofusion

A

Distal prox tubule (outer medulla)

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83
Q

Cystatin C

A

Endogenous cysteine proteinase inhibitor

Good marker of GFR (completely filtered and then reabsorbed)

Urinary Cystatin C may be a good marker for tubular injury (usually none found in the urine)

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84
Q

Fluid of choice in AKI resuscitation

A

Haartmans/ lacted ringers/plasma lyte

  • Less chloride than NaCl
  • Reduced major adverse events
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85
Q

Most important strategy to prevent contrast induced AKI

A

Pre-hydration

Also have protective effect from statins

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86
Q

Ciclosporin

A 
SE:
Nephrotoxicity
TMA/HUS
Diabetes
Hyperlipidaemia
MEtabolic: K+, urate
Neurotoxicity
Myoneuropathy
Hirsutism, gingivial hyperplasia
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87
Q

Tacrolimus/CsA

A

Calcineurin inhibitor
-T cell suppresses

SE:
Less HTN, Hyperlipidaemia, and hyperuricemia than CsA
-Diabetes more than CsA
-Hair loss (Hirsutism w/ CsA)
-Nephro/Neurotoxicity
-Acne
-Malignancy
-TMA
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88
Q

MMF

A

T and B cell targets
MOA: Inhibitor of inosine monophophate dehydrogenase; inhibits purine synthesis; anti proliferative effect on lymphocytes

SE:
GIT
Myelosuppression

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89
Q

Azathioprine

A

T and B cell targets

SE:
GIT
Myelosuppression
Macrocytic changes

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90
Q

Rapamycin (sirolimus/rapamune) and Everolimus

A

m-tor inhibitors

  • Binds to FKBP like CNI but do not act the same way
  • Inhibit T cell activation and proliferation in response to anigenic and cytokine stimulation
SE:
Lipids
Thrombocytopenia
Oedema
Poor wound healing
mouth ulcers
Pneumonitis (sirolimus) 
Fertility issues
Proteinuria
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91
Q

Basiliximab/Daclizumab

A 
IL2 receptor (CD25)
-On T cells

Induction of immunotherapy

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92
Q

ATG/ATGAM/Thymoglobulin

A

Polyclonal T cell depleting antibodies

For induction or rejection

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93
Q

Intrinsic kidney cell injury in IgA

A

Mesangial cells

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94
Q

Intrinsic kidney cell injury in Membranous nephropathy

A

Podacytes

95
Q

Intrinsic kidney cell injury in ANCA GN

A

Endothelial cells

96
Q

Intrinsic kidney cell injury in FSGS

A

Podacytes

97
Q

Intrinsic kidney cell injury in MCD

A

Podacytes

98
Q

Primary Membranous nephropathy Ab

A

PLA2R

THSD7A

99
Q

Secondary causes of membranous nephropathy

A

SLE
HBV/HCV/HIV
Solid organ malignancy (usually lung or colon)
Meds: NSAIDS, Gold, Penicillamine

100
Q

Histo for Membranous Nephropathy

A

Subepithelial spikes
Thickened BM
IgG4 mainly

101
Q

Natural History of membranous nephropathy

A

1/3 complete remission
1/3 partial remission
1/3 Persistent nephrotic syndrome

102
Q

Tx of Membranous GN

A
  1. Ponticelli (Cyclo and pred)
  2. Rituximab or CsA

Usually wait and watch initially unless PLA2R positive and proteinuria >3.5 g/day then immunosuppress

ACE/ARB for proteinuria
Treat underlying cause if secondary

103
Q

SE of Cyclophosphamide

A

Activation of viral hepatitis
Alopecia
Gonadal damage
Hemorrhagic cystitis (due to metabolisation into acrolein)
Neoplasia
Transitional cell carcinoma of the bladder
Toxic hepatitis

104
Q

Histo for MCD

A

LM normal
EM: Diffuse foot process effacement

T cell dysfunction as pathophys

105
Q

Mx of MCD

A

Steroids - most respond in 8 weeks

CNI or RTX second line if frequent relapses

106
Q

Collapsing FSGS is associated with what

A

HIV/ viral causes

107
Q

Effect on albumin in primary vs secondary FSGS

A

Primary have low albumin and secondary usually normal

108
Q

Genetics in FSGS

A

AR

Podocin (NPSH2)

Nephrin(NPHS1)

109
Q

Tx of FSGS

A

Steroids
CNIs if unable to wean

Poor prognosis if persistent proteinuria: >50% ESKD

110
Q

Amyloidosis Histo

A

Congo red staining

Apple green birefringence under polarised light

111
Q

When to anticoagulate in nephrotic syndrome

A

Albumin <20

8 times higher risk of VTE and arterial thrombosis
USually in first 6 months

Esp with membranous GN

112
Q

Which type of IgA is commonly the cause of GN

A

IgA1

-Galactose deficient

113
Q

Strongest risk factor for predicting poor prognosis in IgA GN

A

Proteinuria >1 g per day

114
Q

Mx of IgA GN

A

ACE/ARB
Strict BP control <130/80

Steroids

  • Can consider if >1g protein after 6 mo ACEi
  • Improves proteinuria, but no benefit in egfr, significant toxicity compared to benefit
115
Q

Differentiating MPGN from C3GN/DDD

A

All: Mesangia hypercellularity, endocapillary proliferation, double contour of BM

MPGN: Low C3 and C4 (classical complement pathway)

C3GN/DDD: Low C3 and normal C4 (alternative complement pathway)

116
Q

MPGN with only C3 on IF

A

C3GN

117
Q

MPGN with full house of Ig on IF

A

Lupus

118
Q

MPGN with just kappa and lambda light chains

A

MGUS

119
Q

Tx of C3GN

A

Conservative - ACEi
Known Ab: RTX or Eculizumab
Decreased Factor H function: FFP regularly

120
Q

Histo for Post Strep GN

A

EM: Subepithelial Humps

121
Q

Mx of ANCA vasculitis

A

Induction then maintainence
Steroids + CYC/RTX
AZA for maintainence
-RTX found to be more effective in maintainence though but cost ++

PLEX controversial - used in alveolar hemorrhage

122
Q

Risk factors for relapse in ANCA vasculitis

A

PR3>MPO ANCA
Upper airway or lower airway involvement

10% risk per year

123
Q

Anti GBM GN target

A

Ab against the NC1 domain of the alpha 3 chain of type 4 collagen in the kidneys and lungs

124
Q

Histo for Anti GBM

A

Linear IgG on GBM of kidney biopsy

125
Q

Prognosis for Anti GBM

A

Usually does not recurr - once off episode, but potential for rapid ESRD and 90% mortality if not treated

126
Q

Tx of Anti GBM GN

A

CYC, Pred, and PLEX

127
Q

Class 1 LN

A

Minimal mesangial LN

-No treatment

128
Q

Class 2 LN

A

Mesangial proliferative LN

-No Treatment

129
Q

Class 3/4 LN

A

Focal and diffuse proliferative LN

  • Focal: <50% glomeruli is class 3
  • Diffuse: >50% glomeruli is class 4

Tx:

  • MMF
  • Alt choices: CYC/RTX/AZA
  • Tac and MMF together shown to reduce relapse
130
Q

Class 5 LN

A

Membranous LN

-Treatment controversial

131
Q

Class 6 LN

A

Sclerotic LN

-Too late for treatment

132
Q

Causes for immune complex mediated MPGN

A

Hep C
Subacute bacterial endocarditis
CTDs
Paraproteinemia

133
Q

Complement mediated MPGN

A

Alternative complement pathway

Independent of antigen/antibody stimulus

134
Q

Proliferative LN histo

A 
Subendothelial immune deposits/wire loops
Hypercellularity
Leukocyte infiltration
Fibrinoid necrosis/hyaline thrombi
Deposits of IgG. C1q, C3, IgA, IgM
135
Q

Poor prognostic indicators for proliferative LN

A 
African american/hispanic
Male
Paeds onset
Neuropsych lupus
Proteinuria >4g/day at diagnosis
Frequent relapses
Elevated Cr at presentation
Failure to acheive remission
136
Q

LN and pregnancy

A

Need to be in remission for at least 6 months and switched MMF to AZA for at least 6 weeks prior to conception

Alt drugs: CsA/Tac

137
Q

Kimmelsteil Wilson lesions

A

DN

138
Q

Leading cause of ESRF in the world

A

DN

139
Q

Screening timelines for DN in T1DM and T2DM

A

T1DM - from 5 yrs

T2DM - From diagnosis

140
Q

DN:

ACR levels suggesting macroalbuminaemia

A

ACR:
Males: >25 mg/mmol
Females: >35 mg/mmol

24Hr Albumin >300mg/24hrs

141
Q

Mx of DN

A 
ACE/ARB
--Slow progression
BP control
Glycemic control
SGLT2i (not used if egfr <30)
--Reduce progression, CVS, and CCF admission
CVS risk factors
142
Q

What size of renal stones are likely to pass or not

A

<4 mm pass easily
5-7 mm 50% pass
>7 mm unlikely to pass without intervention

143
Q

Macula Densa physiology

A

Macula densasenses flow and [NaCl]
•
Increase flow or increase [NaCl] increases afferent arteriole contraction decrease GFR
•
Decrease flow or decrease [NaCl] increases afferent arteriole dilatation, efferent constriction increase GFR

144
Q

What is the dialysis paradox

A

Dialysis:

  • Disadvantage with lower BP
  • Advantage with obese patients

Opposite for transplant

145
Q

Indications for EPO as per PBS

A

Hb <100 g/L and

egfr <60 ml/min

146
Q

Target Hb in EPO and complication if too high

A

Hb 100-120

Increased risk of vascular occlusive disease if greater, avoid in solid organ malignancy (EPO is a growth factor)

147
Q

Develop functional iron deficiency with EPO, so what are the Tsat and ferritin aims

A

Tsat 20-50%

Ferritin 300-500

148
Q

Causes of EPO resistance

A 
Absolute/functional Fe deficiency
Infection/Inflammation
Malignancy
Chronic blood loss
Hyper PTH
Malnutrition
Drugs (ACEi)
149
Q

HIF PH inhibitors MOA and indication

A

Mimics normal adaptive response to hypoxia

  • Induces endogenous EPO production by blocking HIF-PH and replicating hypoxic conditions
  • Increases utilisation of dietary iron and reduces EPO resistance

Vedadustat, Daprostat, Molidustat, Roxadustat

150
Q

MOA of renal bone disease

A

Decrease in renal function leads to hyperphosphatemia.

  • Leads to hypocalcemia and increase in PTH
  • Increase in PTH upregulates osteoclast activity
151
Q

ESRF and MOA of vascular calcification

A

hyperphosphatemia leads to retained phosphate binding to calcium and causing vascular calcification

152
Q

Target level for PO4 in ESRF

A

0.8-1.6

153
Q

Target level for Ca in ESRF

A

2.1-2.4

154
Q

Target Level for PTH in ESRF

A

2-3 times UNL

155
Q

Mx of renal Bone disease

A
  1. Phosphate binders
    - -Sevelamer, Lanthanum, Calcium Carbonate, Sucroferric oxyhydroxide (not constipating)
  2. Use calcitriol to titrate up Ca
    - -Measure PTH 2-3 monthly
    - -PTHectomy if autonomous (high PTH and Ca whilst off Ca/Vit D agents)
  3. Calcimimetics (cinacalcet)
    - -No survival benefit, off PBS now
156
Q

Hormones that reduce phosphate

A

FGF23 and PTH

157
Q

Hormones that increase Phosphate

A

Calcitriol via increasing intestinal absorption

158
Q

FGF23

A

FGF23 is a phosphate regulator

  • Released from bone
  • Promotes urinary excretion of PO4 and combats reabsorption of phosphate (by inhibiting vit D production)

-PTH may become elevated with Vit D suppression

Klotho is an important co-receptor

159
Q

How much of the blood flow to the kidney is filtered

A

kidneys have 20% of CO

20% of plasma flow delivered to each nephron becomes filtrate (180L/day)

160
Q

What is the most important determinant of GFR

A

Capillary hydrostatic pressure

Reduced when there is an increase in afferent arteriolar tone or a decrease in efferent arteriolar tone

161
Q

Gold standard for measuring GFR

A

Isotopic GFR (nuclear study)

162
Q

Drugs causing afferent arteriole dilatation (increase GFR)

A

NO

Prostacyclin

163
Q

Drugs causing afferent arteriole constriction (decrease GFR)

A

Angiotensin 2 at high doses
Adenosine
NSAID
Norad

164
Q

Drugs causing efferent arteriole dilatation (decrease GFR)

A

ACE/ARB

165
Q

Signals to JGA

A

Arterial pressure
Venous volume
Fluid delivery to macula densa (nephron autoregulation)

166
Q

JGA effects changes to

A

Renin release

Nephron GFR

167
Q

Main area of renal autoregulation

A
  • Mainly through changes in afferent arteriolar tone (angiotensin 2 acts mainly through efferent arteriolar tone)
  • Adenosine: Afferent arteriole constriction
  • PG and NO: Afferent arteriole dilatation
168
Q

Mechanism of renal autoregulation

A
  1. Myogenic mechanism - afferent arteriole contraction via endothelin
  2. Tubuloglomerular feedback
    - Na and Cl concentration at macula densa increased, afferent tone is increased and GFR falls
169
Q

Effects of Angiotensin 2

A 
Increase SNS
Increase PT Na reabsorption
Increased Aldosterone secretion
Arteriolar vasoconstriction
Increased ADH secretion
170
Q

Water reabsorption

A

Mostly in PT, small amount in decending thin limb, and variable in CD (regulated by ADH)

171
Q

Sodium reabsorption

A

Mostly in PT, then ascending thin and thick, and little in CD

172
Q

What is absorbed in the proximal tubule

A 
Water
Sodium
Most of the bicarb
All glucose
All amino acids
Most phosphate
173
Q

Proximal Tubule Transporters

A

Basolateral:
Na/K ATPase
HCO3, Organic, K+ (in)

Apical:
NA/Organic co transporter
Na/Amino acid cotransporter
Na/Phosphate cotransporter
Na/H+ exchanger (H+out)
174
Q

MOA of Frusemide

A

Blocks NA/K/Cl co transpoter on apical portion of thick ascending limb and prevents those electrolytes from being reabsorbed

175
Q

Where is the most dilute luminal fluid in the nephron

A

thick ascending loop

Critical part of nephron for electrolyte reabsorption and regulation of body osmolality

176
Q

Transporters in the distal tubule

A

Basolateral

  • Na/K ATPAase
  • Na/Ca counter transporter (Ca in)

Apical:
Na/Cl cotransporter (in)
Calcium channel (in)

177
Q

MOA of thiazide

A

Blocks the NA/Cl cotransporter in the distal tubule

-Leads to increased Na excretion and decreased Ca excretion

178
Q

MOA of thiazide/Indapamide/Metolazone

A

Blocks the Na/Cl cotransporter in the distal tubule (NKCC1)

-Leads to increased Na excretion and decreased Ca excretion

179
Q

Collecting Duct and Late distal tubule transporters

Principal cell

A

Principal Cell

  • Basolateral:
  • -Na/K ATPase
  • Apical:
  • -Na EnaC channel
  • -ROMK apical K channel

Principal area of aldersterone effect (increases production of Na EnaC channels)

180
Q

MOA Spironalactone

A

Blocks the aldosterone cytoplasmic receptor binding in the principal cells of the CT/late distal tubule

Decreases a reabsorption and increases K and H+ retention

181
Q

MOA Ameloride

A

Blocks EnaC channels on apical surface of CT/late distal tubule in the principal cells

Results in decreased Na absorption and increased K+ and H+ retention

182
Q

Collecting Duct and Late distal tubule transporters

Intercalated cells type A

A

Secretes H+ and reabsorbs HCO3

183
Q

Collecting Duct and Late distal tubule transporters

Intercalated cells type B

A

Secretes HCO3 and reabsorbs H+

184
Q

Medullary collecting duct

A

Permeability controlled by ADH

Has permeability for urea unlike cortical CT

185
Q

Potassium reabsorption

A

PT and thick ascending loop of henle

Regulated in the late distal tubule/CT under influence of aldosterone

186
Q

Potassium regulation

A

High plasma aldosterone increases K+ secretion

Alkalosis leads to hypokalemia due to H+/K+ exchange

187
Q

Calcium reabsorption and regulation

A

Reabsorbed in PT and ascending thick limb, and a little in CT

Regulated in thick ascending loop of henle and distal tubules via PTH

188
Q

TMA definition

A

MAHA

  • RBC fragmentation passing through thrombus laden small vessels
  • Schistocytes
Thrombocytopenia
Organ injury (AKI)
189
Q

Haemolytic anaemia + thrombocytopenia +Coombs positive =

A

Evan’s syndrome

190
Q

Haemolytic anaemia +thrombocytopenia +Coombs negative =

A

TMA

191
Q

CAuses of TMA

A 
TTP
aHUS
HUS
SLE/APLS
Pregnancy
Cancer
HIV
Drugs
192
Q

Cause of TTP

A

ADAMTS13 deficienct (<5-10% activity) leading to vWF multimers

Usually due to an acquired Ab

193
Q

Tx of TTP

A

PLEX to remove Ab

FFP to correct ADAMST13 def

194
Q

Mx of HUS

A

Supportive

195
Q

Factor H and I

A

Regulate the complement Alternative pathway

196
Q

Cause of aHUS

A

Usually loss of function mutation in regulator of alternative pathway such as factor H and I

Can be a gain of function mutation

Or Anti Factor H antibodies

Often have a trigger infection (pregnancy, infection)

197
Q

Anti Factor H antibodies gene

A

CFHR1-2 deletion

198
Q

Tx of aHUS

A

Eculizumab ASAP

PLEX has no benefit

199
Q

Clinical picture of TMA vs HUS/aHUS

A

TMA:

  • Plt <30
  • Neuro involvement
  • AKI mild-mod

HUS/aHUS:

  • Plt >30
  • Less neuro
  • Severe AKI
200
Q

PNH mutation

A

PIG-A gene

  • Clonal deletion of GPI anchor which binds CD55 and CD59 to cell surface (complement inhibitors)
  • Without this complement destroys RBCs
201
Q

Tx PNH

A

Eculizumab

202
Q

Cut off egfr for SGLT2 use

A

egfr >30

203
Q

Evidence for statin in CKD

A

Reduced CVS in non dialysis patients

204
Q

SGLT2 presurgery

A

W/H 2 days prior to OT and resume when eating again

205
Q

SGLT2 in CKD

A

Reduces progression to ESRF in patients with CKD/albuminuria

Most effective in macroalbuminuria

Reduces hyperfiltration via tubuloglomerular feedback

206
Q

Riskfactors for progression of ADPKD

A 
Age
GFR and rate of decline
Male
HT before age 35
PKD1 mutation
Total kidney volume (on MRI)
207
Q

Mx of ADPCKD

A

Aim home BP <110/75 in age <50, egfr >60 ad no CV disease

Tolvaptan (V2 receptor antagonist)

208
Q

The worse predictor of poor outcome on the MEST C score for IgA GN

A

Tubular atrophy/interstitial fibrosis (IFTA)

209
Q

Cellular rejection Histo

A

T cell mediated

Tubulitis, interstitial inflammation

210
Q

Histo features of AMR

A

Peritubular capillaritis without tubulitis, vasculitis, C4d staining, Glomerulitis

211
Q

CNI Nephrotoxicity features

A

Isometric vacuolation tubular epithelial cells

  • Striped intersitial fibrosis
  • Nodular hyalinosis (also in HTN and diabetes)
212
Q

Hyperacute Rejection cause

A

High level preformed DSA or high level haemaglutinins (Anti-A and B)

PLEX can be trialled to remove DSA

213
Q

Most important HLA matches that are tested in Renal Tx

A

A, B, DR

Score out of 6

214
Q

AMR Rx

A

PLEX/IVIG

Repeat Bx at 2 and 4 weeks, if ongoing AMR - RTX, Rescue Splenectomy, High dose IVIG

215
Q

Most significant long term problem with Renal Tx

A

Chronic AMR

216
Q

Main finding associated with long term renal allograft failure

A

IFTA

217
Q

Oncogenic Viruses: HHV-8

A

Kaposi’s Sarcoma

218
Q

Oncogenic Viruses: EBV

A

Lymphoma (PTLD)

219
Q

Oncogenic Viruses: HBV

A

Hepatoma

220
Q

BK virus Diagnosis and Mx

A

Decoy cells in urine
BK PCR
Bx: SV40 stains, resembles acute rejection

Tx: Reduce immunosuppression, switch to mTOR etc.

221
Q

Site in nephron for SGLT2 action

A

Proximal tubule

222
Q

Gene associated with FHHNC

A

Claudin 16

PResentation: Hypomag, Hypercalciuria, Nephrocalcinosis

223
Q

Bartter’s Syndrome

A 
AR
Thick ascending loop of henle
Normotensive
Hypokalemia
metabolic alkalosis
HYPERCALCURIA (Different from Gittleman's)

Dx: Increase in urine Prostaglandin E

Presents in neonates

224
Q

TRPM6

A

Channel for Mg absorption in distal tubule that can be blocked by tacrolimus

225
Q

TRPV5

A

Channel for calcium absorption in distal tubule

226
Q

Gitelman’s syndome

A 
AR
Normotensive
metabolic alkalosis
Hypokalemia
HYPOCALCURIA (similar to thiazide) - Loss of function of NKCC1 channel

Presentation in childhood/adults

227
Q

Gordon Syndrome (Pseudohypoaldosteronism Type 2)

A 
AD
HTN 2nd/3rd decade
NAGMA
Hyperkalemia
Hypercalciuria

Tx: Thiazides (mirror image of thiazide use - upregulation of NKCC1)

228
Q

Liddle Syndrome

A 
AD
HTN 
Hypokalemia
Metabolic alkalosis
Increased ENac channels

Tx: Amiloride, Triamterene

229
Q

Diagnosis of ADPCKD

A
  • 15-39YO > 3 unilateral or bilateral cysts *specificity and PPV 100%
  • 40-59YO - > 2 cysts in each kidney
  • 60YO or older - > 4 cysts in EACH KIDNEY
230
Q

MOA Acetazolamide

A

Carbonic anhydrase inhibitor

In Proximal tubule

231
Q

RTA Type 1

A

Impaired ability to excrete H+ in distal tubule

  • Urine pH >5.5
  • Stones/Hypercalcemia
  • Hyperchloremic acidosis
  • -Bicarb <15

Cause:
-SLE, Sjogrens, amphoterecin

232
Q

RTA Type 2

A

Impaired HCO3 reabsorption in prox tubule

  • Urine pH >5.5
  • Hyperchloremic acidosis
  • Plasma Bicarb usually >15

Cause:
-MM, Acetazolamice, Fanconi syndrome, Vit D deficiency, Hereditary hypercalciuria

MX: Bicarb

233
Q

RTA Type 4

A

DEcreased secretion of aldosterone or decreased effect

  • Urine pH <5.5
  • Hyperchloremic acidosis
  • High K+
  • Bicarb >15

Cause:
-Aldosterone deficiency, NSAIDS, ACEi, ARB, Spiro

Mx: Dietary sodium restriction, frusemide

Bpt (15 decks)

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