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Renal Flashcards

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1
Q

Define Nephrotic Syndrome:

A

Criteria is:
*Proteinuria >3.5g/ 24hours

  • Hypoalbuminemia <30g
  • Oedema

[Must have all these!!]

additional features are:

  • hypogammaglobulinemia
  • Hypercoagulable
  • hyperlipidaemia
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2
Q

List some things that can effect creatinine levels:

A

Muscle mass

Concentration of plasma
- dehydration

Secretion of creatinine ~15% secreted

Diet
- high protein may increase it slightly

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3
Q

What things can effect urea levels?

A

G.I bleeds

Dehydration

Liver failure
- low urea

Increased tissue breakdown
- steroids

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4
Q

What does eGFR take into account?

A

Plasma creatinine
Age
Gender
Race

expressed as GFR expressed as ml/min 1.73m2

MDRD - the method used.

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5
Q

How much can kidney function drop by before the creatinine level rises?

A

50%

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6
Q

What does eGFR not take into account?

A

Acute injury to kidneys.

this is because muscle mass takes time to build up levels.

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7
Q

What are the stages of CKD?

A

Stage 1:
>90, with other abnormality

Stage 2:
60-89, with another abnormality

Stage 3:
30-59

Stage 4:
15-29

Stage 5:
<15

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8
Q

If a person has glomerulonephritis, will both kidneys be affected?

A

Yes.

but maybe not all of the kidney will be affected.

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9
Q

What is needed to make a diagnosis of glomerulonephritis?

A

Biopsy

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10
Q

What tests are done during biopsy?

A

Light microscopy
- glomerular and tubular structure

Immunofluorescence
- looking for IgG

Electron Microscopy
- deposits on membrane

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11
Q

What will be seen with Rapid Progressing Glomerulonephritis?

A

Crescent formation of the glomeruli membrane

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12
Q

List the stages that occur leading to glomerulonephritis, and the possible therapeutic strategies that can be done:

A
  1. Insult
    - infection
    - antibody
  2. Injury
    - Block Ab
  3. Response to Injury
    - Steroids
    - cytotoxics
  4. Outcome
    - dialysis
    - transplantation
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13
Q

What is the most common primary nephritis?

How does it present?

A

IgA nephropathy
- minor urinary abnormalities

  • Hypertension

Renal impairment

Can be rapidly progressing

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14
Q

What is IgA nephropathy?

A

Mesangial disease - proliferation leading to failure of the kidney.

there is deposits of IgA with complement activation.

often presents with Strep infection - Synpharyngitic infection.

its also associated with:

  • liver disease
  • coeliac disease
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15
Q

What is Membranous Glomerulonephritis?

A

Disease of adults - specifically caucasians.
Most common cause of nephrotic syndrome

Associated with:

  • lung cancer
  • prostate cancer

Due to [Anti- phospholipase A2 Receptor] located on the podocytes.

Immune complex deposition within the deposts.

Variable nature:

  • third spontaneous remission
  • Third progress to ESRF
  • third progress to persistent proteinuria

Treatment:
Primary:
- control blood pressure
- immunotherapy - steroids, cyclophosphamide, cyclosporin

Secondary
- treat underlying condition

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16
Q

What is minimal Change disease?

A

Commonest cause of nephrotic syndrome in children
- so common unlikely to biopsy because likely to be this.

Disorder of the podocytes. - where you get fusion of the podocytes.
T - cell mediated disease

Associated with:
- Hodgkin’s

Associated with:
- URTI

Relapsing disease

Treatment:
- steroids

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17
Q

Crescentic Disease:

A

Rapidly Progressive Glomerulonephritis
- group of conditions that cause crescents on kidney biopsy

ANCA Vasculitis - MPO 
Lupus 
Good Pastures disease  - anti GBM 
Infection Associated 
Henoch -Schonlein Purpura
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18
Q

What nodules are seen with diabetic nephropathy?

A

Kimmelstiel wilson nodules

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19
Q

Why are angiograms and contrast CTs not done in renal disease?

A

Due to the contrast agents which can contraindicate in renal disease.

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20
Q

Where does the hypoxia first occur in renal system in renal stenosis?

A

Cortex - most metabolically active part

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21
Q

What are the two ways you can lose albumin?

A

Renal

Bowels

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22
Q

What is the diagnostic tests for Amyloidosis:

A

Congo Stain

  • Apple green bifridgence
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23
Q

What is the treatment for lupus?

Study These Flashcards
A

Steroids
Cyclophosphamide
Rituximab

24
Q

Whats the gold standard for assessing renal scars?

25
What is MAG3 cystogram used?
Used for | Vesicoureteral Reflux
26
Outline the grades of Vesicoureteral Reflux:
Grade 1: - urine just makes it half way up ureter Grade 2: - Urine into the pelvis Grade 3: - dilatation of the pelvis Grade 4: - Torturous process of ureters and dilation Grade 5: - Massively tortuous and dilated.
27
When can | Vesicoureteral Reflux be picked up?
In utero After infection
28
Whats the management for Vesicoureteral reflux:
Prophylaxis antibiotics Surgery: - STING procedure - circumcision
29
What is another common obstruction that can occur in children which involves faulty valves, and how does it present and how is it managed?
Posterior Urethral Valve Presentation: - Antenatal Hydronephrosis - UTI - Poor Urinary Syndrome Management: - Valve resection - antibiotic prophylaxis - CKD care Outcome: - Chronic renal failure
30
Whats the most common cause of hydronephrosis in children?
Pelvi - Ureteric Junction Obstruction Managed with: - Pyeloplasty
31
What is the most common congenital kidney disease?
Adult polycystic kidney disease - Autosomal dominant condition Caused by: - PKD1 - Chromosome 16 - PKD1 - Chromosome 4 kidneys increases massively. Diagnosed: - Ultrasound 2 cysts need bilaterally in 15-30 years old. Outcome: 50% risk of ESKD by 50 years Cyst accidents - rupturing. Management: - supportive - treat complications - Dialysis - Dialysis * Tolvaptan - reduces cyst formation - since its V2 antagonist they pass lots of water
32
Name an inherited kidney disease that effects the collagen 4:
Alport's syndrome x-linked disease Collagen 4 abnormalities Symptoms: - renal - deafness
33
Name an inherited kidney disease which effects storage defects;
Fabry's disease Angiokeratoma - associated skin pathology. Alpha Gal A defect
34
In someone with Minimal change disease what investigations would you carry out?
Urinalysis - high protein ++++ - urine/ creatinine ratio Serum albumin level Coagulative factors - often antithrombin is released GFR Serology - ANA - ANCA - Anti GBM Renal ultrasound - not just checking for blockages - assessing kidney size - checking there is two kidneys Chest - xray - pulmonary oedema - signs of hodgkins
35
List some negative aspects of using eGFR:
Non- linear relationship but is expecnitional to kidney function. - only starts to rise after 50% loss of kidney function Overestimates kidney function in people with low muscle Under estimates kidney function in people with large muscle mass it is not useful for acute kidney failure - there could be 0GFR and the creatinine would be normal until sufficient levels build up It is inaccurate above eGFR >60. due to the studies it was conducted in It is inaccurate in children - due to studies of people it was studied and developed in.
36
What is some complication that can occur in people who are treated for glomerulonephritic conditions?
Infections - due to the high use of immunosupressants namely - peritoneal infections in nephrotic patients. *due to the movement of fluids
37
What complications can occur in nephrotic syndromes?
Clots - due to lack of anti-thrombin III - painful legs Pulmonary Oedema - due to lack of Albumin to maintain oncotic pressure Infections - Hypoglobulinemia
38
In chronic kidney disease, why would you stop Thiazide diuretics?
Side effect is hyperuricaemia - thus in someone already prone to having high urea this could be dangerous
39
Outwith direct analysis of the kidney, what other tests would you do to investigate someone with nephritic syndrome?
Chest - x- ray - checking for pulmonary edema Sepsis check - these patients are hypoalbuminemic and predisposed to pneumococcal infections Coagulation tests - loss of antithrombin III leaves these people predisposed to clots Lipid tests - the liver secretes a high amount of lipids
40
List some symptoms of AKI:
Oliguria Oedema build up - around eyes and feet Tachypnea Confusion Nausea Chest pain
41
List some medications associated with causing AKI:
Diuretics - dehydration ACE and NSAIDs - dysregulated autoregulation of the kidney Gentamicin - Acute tubular necrosis Opiates - blockage of the ureters **usually it is a compensation or in the setting of damage kidneys already
42
What is the Investigations in AKI:
Past medical history is absolutely key, to establish anything that may suggest hypovolemia or sorts. Acute vs Chronic - e-alert changes FBC: - signs of anaemia - Hypocalcaemia * these are suggestive of long standing renal failure U&Es - specifically K+ levels - lack of excretion of K+ can lead to hyperkalemia Urine output Urine analysis Osmolality of blood and urine ABGs - looking for acidosis - which can be common due to lack of filtration and excretion of H+ Underlying diagnosis - ANCAs - ANAs - IgA - volume stasis Ultrasound - establish post renal causes ECG - for hyperkalemia
43
What is your management of AKI?
ABCS Pre-renal: - fluid - hartmann's or saline Remove causes - sepsis treat - drug causes - remove drugs Remove obstructions * *treat hyperkalemia - this is what is likely to kill Dialysis if not improving - refractory hyperkalemia - Refractory pulmonary oedema
44
What features would you expect to see that suggest hyperkalemia and how would this be treated:
Tall T waves Flattening of P waves Prolongation of P- R interval Broad QRS - late component Treatment: - Calcium resonium (stops absorption in the G.I) - Insulin - actarapid +/- - Glucose - Calcium gluconate (protects Membrane, less likely to be activated by K+ Treat Acidosis - bicarbonate (patients are likely to become acidotic in AKI due to failure of H+ secretion and HCO3- reabsorption - acidosis increases K+ build up) Dialysis - if needed
45
What drugs are associated with tubular necrosis and should be stopped immediately in AKI?
Gentamicin NSAIDs ACE Contrast Poisons **note some of these cause necrosis through dysregulation of blood flow and some cause it through direct toxicity
46
What biochemical marker will be elevated in Rhabdomyolysis?
Serum Creatinine
47
What side effect may Sulphonylureas or Insulin therapy have in CKD?
Kidneys play a role in insulin metabolism - therefore drugs increasing their level the person more predisposed to developing hypoglycemia
48
Name some common causes of CKD:
Vascular: - HTN - Renal sclerosis - Diabetes Congenital: - Polycystic kidney disease - Congenital Obstructive Uropathy Glomerular disease: - Lupus - Amyloidosis - Wegner's Tubulointerstitial disease: - drug toxicity - TB Urinary Tract obstruction - Calculus disease - Prostatic disease
49
List some symptoms of CKD and why are these?
Symptoms usually refer to the build up of toxic metabolites: - malaise - Loss of appetite - nocturia (due to impaired ability to concentrate urine) - itching - nausea - restless legs Advance stages: - Pericardial rub (urea irates the pericardium) - Encephalopathy
50
What is the management of CKD:
Control of Blood pressure Diabetic control
51
Overview some common lab abnormalities seen in CKD:
Hyperkalemia - lack of excretion and acidosis Hypocalamia - no Vit D activation and Increased Phosphate Anemia - No EPO drive
52
CKD can cause bone destruction due to secondary hyperparathyroidism, what is this referred to as?
Renal Osteodystrophy
53
What drug can be used as a synthetic EPO?
Darbepoetin Alfa
54
What may cause a false positive for haematuria in the setting of AKI?
Rhabdomyolysis it is myoglobin from muscle break down that is found in the urine and is nephrotoxic.
55
Why is albumin lost during nephrotic disease?
There is loss of the negatively charged basement membrane
56
What is a drug that can elevate the creatinine and how does it do this?
Trimethoprim blocks excretion of creatine in DCT
57
In pre renal AKI, what would you expect the urine osmolality to be?
HIgh - the kidneys will be concentrating the urine as much as possible

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