Nephrology Investigations Flashcards by Aboudi el masri

Define AKI

Abrupt reduction in kidney function resulting in the retention of nitrogenous products (urea) + dysregulation of electrolytes

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What staging tool is used in nephrology to asses for:
AKI
CKD

Both use KDIGO staging although there are different parameters for both obv

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What is considered reduced urine output?

<0.5 ml/kg/hr

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Run me through the KDIGO staging for AKI

Stage 1:
Serum creatinine >1.5x baseline or >0.3mg/dl within 48hrs
OR Reduced urine output for 6+ hours

Stage 2:
Serum creatinine >2x baseline
OR Reduced urine output for 12+ hours

Stage 3:
Serum creatinine >3x baseline or >4mg/dl
OR Anuria/Reduced urine output for 24+ hours

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What is the GFR of a patient who is not producing any urine? This patient has an eGFR of 10

Anuria is GFR of 0 regardless of what eGFR is

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Drugs are typically eliminated via kidney excretion. Certain drugs have an increased risk of causing AKI and should have their doses appropriate to the patient’s kidney function Give 3 pre-renal and 3 intra-renal drugs leading to AKI.

Pre-renal:
Drugs affecting kidney perfusion (ACE inhibitors!!!, NSAIDs, Diuretics)

Intra-renal:
Nephrotoxins (Gentamicin, Vancomycin, contrast media, chemotherapy drugs)

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What are the Pre-renal causes of AKI

Pre-Renal (reduced supply)
1) Hypovolaemia (cardiogenic/neurogenic/haemorrhagic shock)
2) Sepsis
3) Congestive HF
4) Renal artery stenosis
5) ACE inhibitors!!!

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What are the Intra-renal causes of AKI

Renal:
1) Ischaemia
2) Nephrotoxins (Gentamicin, Vancomycin, contrast media, chemotherapy drugs)
3) Glomerulonephritis
4) Interstitial nephritis
5) Hepatorenal syndrome
6) HUS/TTP

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What are the Post-renal causes of AKI:

Post-Renal: obstructive
1) Nephrolithiasis
2) Tumour obstruction
3) Prostate hypertrophy/tumour
4) Blocked
5) Catheter/outflow obstruction

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What is Hepatorenal syndrome?

What will show on blood tests supporting this?

Conditioned characterised by a rapidly progressive (type 1) or gradual (type 2) decline in kidney function in patients with advanced liver disease such as cirrhosis or acute liver failure.

This deterioration is due to splanchnic vasodilation and renal vasoconstriction

Like any other decline in renal function. Raised creatinine and urea as well as reduced urine output and GFR

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Give 10 causes of AKI

Pre-Renal (reduced supply)
1) Hypovolaemia (cardiogenic/neurogenic/haemorrhagic shock)
2) Sepsis
3) Congestive HF
4) Renal artery stenosis
5) Drugs affecting kidney perfusion (ACE inhibitors!!!, NSAIDs, Diuretics)

Renal:
1) Ischaemia
2) Nephrotoxins (Gentamicin, Vancomycin, contrast media, chemotherapy drugs)
3) Glomerulonephritis
4) Interstitial nephritis
5) Hepatorenal syndrome
6) HUS/TTP

Post-Renal: obstructive
1) Nephrolithiasis
2) Tumour obstruction
3) Prostate hypertrophy/tumour
4) Blocked
5) Catheter/outflow obstruction

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Define CKD

Abnormalities of kidney structure and function for >3 months

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How would you assess kidney function and damage? Give 5 methods

GFR (best for kidney function)
ACR/PCR (Best for kidney damage)
Urinary sediment abnormalities
Imaging abnormalities
Biopsy/histological/pathological abnormalities

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The KDIGO tool is used to grade kidney function and damage. Run me through it

ACR - Damage
A1 - Normal <3.4
A2 - Moderately increased 3.4-34
A3 - Severely increased - >34

eGFR - Function
G1 - Normal - 90+
G2 - Mild increase - 60-89
G3 - Moderate decrease A - 45-59, B - 30-44
G4 - Severe Decrease - 15-29
G5 - ESKD (kidney failure)

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Give 10 causes of CKD

Glomerular -> Diabetes, Sepsis, Autoimmune, Drugs, neoplasia

Vascular -> Atherosclerosis, HTN, Ischaemia, Vasculitis

Tubulointerstitial -> UTI, Nephrolithiasis, Obstruction (BPH, prostate/bladder cancer)

Genetic -> ADPKD, Alport

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What is in a U&E?

Creatinine
BUN
Calcium
Phosphate
K+
Na+

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You obtain results from a U&E which show a disproportionately raised Urea but relatively normal eGFR and creatinine. What is this suggestive of?
Why?

A disproportionate rise in urea compared to creatinine suggests hypovolaemia, a pre-renal cause of AKI

This is because in hypovolemic patients, water, Na, and Urea are increasingly reabsorbed in the PCT giving a rise in urea without a decrease in eGFR

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T or F: Creatinine is used to calculate eGFR because it is solely excreted as is from serum to elimination

False, some is also secreted in the PCR and hence as eGFR decreases, creatinine increases

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Creatinine is neither excreted nor metabolised by the kidney and hence used to measure eGFR. There is, however some secretion in the PCT. Early falls in eGFR may not increase serum creatinine and hence not the best for early renal disease nor in AKI (hence why we dont use eGFR when discussing AKIs). What are some factors affecting serum creatinine levels? Give 3

Remeber creatinine is used to calculate eGFR => think of factors that may influence the calculation
1) Age, Gender, Race
2) Muscle mass/protein-rich diet
3) Ingestion of Red meat within 12 hours
4) Pregnancy

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What are the 2 most used methods of estimating eGFR?

CKD-EPI equation (takes into acount creatinine, age, and gender)
24 hour creatinine clearance

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Muscle mass, protein-rich diet, and red meat consumption affects creatine levels. What tool will you use to estimate eGFR in a patient with these factors?

CockCroft-Gault

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What does a Urine Dipstick detect?

Proteinuria
Haematuria
Haemoglobinuria
Glycosuria
Ketones
Bilirubin
Urobilinogen
Leukocytes
Nitrites
Specific gravity

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What is the difference between haematuria and haemoglobinuria

Haematuria is the presence of blood in urine
Haemoglobinuria is the presence of haemoglobin in the urine (After RBC breakdown)

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Nephrotoxic drugs can lead to what type of AKI? (not pre-renal/intrarenal…)

Acute tubular necrosis

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What is the significance of Haemoglobinuria (what does it indicate)?

Free haemoglobin in the urine suggests intravascular haemolysis such as TTP, DIC, prosthetic valve etc.. This is significant as haemoglobin is nephrotoxic and hence can lead to acute tubular necrosis/AKI

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You are performing a urine dipstick showing ketones. Give 5 ddx

Dehydration!!
DKA
Starvation
Alcoholism
Pre-eclampsia/eclampsia
Hyperthyroidism

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You note high levels of bilirubin on urine dipstick. What does this indicate?

Hepatic disease (Hepatic) or billiary obstruction (post-hepatic) Why? as theyre both conjugated.

What is Urobilinogen? When would it be reduced?

It is the normal metabolism of bilirubin in the duodenum before being reabsorbed in the blood stream and excreted in the urine via the kidneys

this is reduced in post-hepatic (obstructive causes)

(it is the precursor of urobilin which gives the colour of the urine) Low urobilinogen is due to the fact that bile is obstructed => no metabolism of bile into urobilinogen => less being absorbed back in the blood and hence less excreted into the urine to show up in the dipstick

In most UTIs, there will be a presence of haematuria, leukocytes and nitrites. Why are there nitrites?
What organism is known to be -ve for nitrites?

It is due to G-ve bacteria metabolism of urinary nitrates into nitrites

Enterococci are known not to produce these metabolites

Urine microscopy is often used to look for casts/crystal. What are the 3 most common findings? What disease are they most associated with?

RBC casts: Glomerular disease
Muddy brown granular casts/crystals: Acute tubular necrosis
Hyaline casts: normal after exercise or dehydration but not indicative of kidney disease

What are the main causes of Acute Tubular Necrosis? Is it Pre-renal or Intra-renal

It is divided into Ischaemic and Nephrotoxic causes

Ischaemic: Hypotension/shock, severe dehydration, major surgery, trauma, or HF

Nephrotoxic: Gentamicin, Vancomycin, NSAIDs, Contrast agents, myoglobin (rhabdomyolysis), heavy metals etc…

Although it sounds like this is a pre-renal cause as it is affecting the blood supply to the kidneys like the other pre-renal causes, This is an intra-renal cause because there is actual structural damage to the kidney itself (which then sloughs off cells and clog the kidney etc..). In pre-renal there is reduced perfusion but without structural damage (AKA reducing the filtration rate)

What is the BUN:creatinine ratio?
How is it obtained?

Blood Urea Nitrogen/creatinine => blood

What casts are obtained in a case of acute tubular necrosis vs a pre-renal cause of AKI?

Pre-renal: Normal/hyaline
ATN: Muddy Brown Casts

What non-biochemical test/procedure can you perform to differentiate between a pre-renal AKI and acute tubular necrosis?

Response to fluid challenge:
Pre-renal will have a good response (cuz its typically due to factors leading to reduced perfusion of the kidney leading to AKI)

ATN: Poor response

Pre-renal AKI and ATN are often hard to distinguish clinically due to the fact they have such confusingly similar etiologies. What 5 tests are best ordered to try and support one way or the other?

For 4/5 must say raised or low in each, 5/5 must say numbers of the following:
3 Urine:
Urine Sodium
Urine Osmolality
!!Urine Sediment (microscopy)

Blood: BUN:Creatinine ratio

Fluid challenge: Response to fluid challenge

You are concerned of rhabdomyolysis as a cause of AKI. What test will you order?

Creatine kinase (raised)

What will you order as part of your autoimmune serology bloods for the investigation of AKI/CKD?

Which ones are applicable to a glomerulonephritis screen?

Any: ANA, ANCA, Anti-GBM, C3+C4, SPEP, Anti-PLAR2

Glomerulonephritis screening (!!ASOT, Anti-GBM, C3+C4, Hepatitis)

Is PTH its own test? or is it grouped with something else?

It is its own test

What will you send to microbiology regarding the investigation of AKI/CKD?

Blood cultures, Urine M,C&S

What imaging will you perform as part of your investigation along with its escalation.

Renal US (always first line)
CTKUB
MRI/MR angiography
then biopsy (not imaging)

What is the preferred imaging technique used for hydronephrosis?

US kidney

You are investigating a patient with suspected AKI/CKD. You order a renal US as that is the first line imaging investigation. In general what are you looking for

Renal Us to look for the size and structure of the kidney as well as the presence of any obstruction

What imaging modality is best to detect stones, massess and anatomical abnormalities

CTKUB although Renal US should still be performed first

What is the best imaging technique used to help exclude pre-renal causes such as renal artery stenosis and thrombosis?

MR angiography

You are in a long case, there is a patient presenting with clear signs of kidney disease. What investigations will you order/perform for any case (include rationale for each for 5/5)?
State those that are exclusive for CKD (without explanation)

No need to be perfect for 5/5. It just needs to be said quickly and the vast majority included with their justification
Bedside:
ABG (Lactate, acidaemia)
Urine dipstick (protein, blood, leukocytes)

Urine:
Urine M, C&S (casts/crystals, infection)
Urine ACR/PCR

Bloods:
1) U&E - For urea, creatinine and electrolyte imbalances
2) FBC - Infection, anaemia, platelet abnormalities
3) LFT - Rule out liver involvement, particularly hepatorenal syndrome
4) Coag profile -> Clotting/bleeding risk (cause of haematuria) - Imp. in thrombotic microangiopathy or DIC!
5) Autoimmune serology (ANA, ANCA, Anti-GBM, C3+C4, hepatitis, Anti-GBM, AntiPLAR2)
6) Creatine Kinase (Rhabdomyolysis) -ACUTE ONLY
CHRONIC ONLY:
7) Fasting glucose/HbA1c
8) Glomerulonephritis screen (ASOT, C3,C4, Hepatitis, Anti-GBM)
9) Bone profile
10) PTH
11) Iron study, B12, Folate

Micro: Blood cultures, Urine M,C&S

Imaging:
Renal US: Always first line assessing for size, structure, and obstruction
CT KUB: Best for assessing obstruction, masses, and structural abnormalities
MRI/MR angiography/renal arterogram: Assesses vascular causes such as Renal artery stenosis or thrombosis

Procedure: Kidney biopsy

Which occurs first? Diabetic kidney disease or diabetic retinopathy

Diabetic retinopathy.
Diabetic kidney disease typically occurs 5-10 years after diagnosis and after diabetic retinopathy begins to ensue

What is the most likely diagnosis of a patient presenting with end-stage kidney disease on a background of uncontrolled hypertension?

Hypertensive Nephrosclerosis

A patient comes in with a history of HTN that is suddenly uncontrolled. They have a history of atherosclerotic disease.
Kidney Us shows asymmetrical kidney size with a difference of 2.5cm compared to the contralateral side. MR angiography/renal arterogram shows renal artery luminal narrowing. What is the most likely diagnosis?

Given the most likely diagnosis, what other scan may be ordered to support your diagnosis? What will it show?

Note that in this case it is suddenly uncontrolled => AKI compared to a CKD chronic case in the case of hypertensive nephrosclerosis
Dx: Ischaemic nephropathy

A duplex scan of the renal artery shows increased resistance

A man is presenting with R-sided flank pain. They have displayed hesitancy, increased urinary frequency, double voiding and nocturia. Kidney US shows hydronephrosis.

Give 3 ddx
What is the overlying term used to encompass these ddx?
What additional imaging can be used to support your diagnosis?

Prostatic enlargement (BPH, malignancy)
Bladder obstruction (tumour, vesicoureteric reflux, abscess, stones)
Renal stones

Obstructive Uropathy

Post-void residual (>50ml)

Is post-void residual done at the bedside or at the radiology department?

Bedside

What is AntiPLAR2?
What is it used to diagnose

Antiphospholipase A2 receptor antibodies
It is a serology test used to diagnose membranous nephropathy

Why would you perform serology for HIV in the setting of kidney disease?

Nephrotic syndrome specifically focal segmental glomerulonephritis

Why would you perform serology for Hep B&C in the setting of nephrotic syndrome?

Membranous nephropathy

Why would you perform SPEP in the setting of kidney disease?

Multiple Myeloma
Amyloidosis

What lab results will be most consistent with nephrotic syndrome?

What are additional tests to perform if suspecting nephrotic syndrome

24-hour urine collection >3.5g in 24hr
PCR >300
ACR >250

Primary causes: Biopsy and serology for AntiPLAR2 (membranous nephropathy)

Secondary causes: serology for:
SLE -> ANA
Focal Segmental Glomerulonephritis - HIV
Hep B&C -> membranous nephropathy

A patient presents with sudden onset hypertension without a history of HTN. They also have raised creatinine and haematuria. On examination they have a rash and signs of arthritis including joint pain.
Urinalysis shows haematuria + proteinuria
Microscopy shows RBC casts

What is the most likely diagnosis?

How will you confirm the diagnosis?

What is the relevant serology?

Given the most likely diagnosis give 2 other causes

Glomerulonephritis

Kidney biopsy (confirms type as well)

Serology: ASOT, C3,C4, Hepatitis, Anti-GBM

Post-infectious: HUS (if +bloody diarrhoea), Recurrent pharyngeal or cutaneous infection

What are the 2 most likely organisms to cause HUS?

Shigella
STEC: Shiga toxin Ecoli

Give 4 mechanisms enabled by CKD to cause the patient to become anaemic

1) EPO deficiency (esp stage 3+)
2) Fe deficiency
3) Anaemia of chronic disease (vasculitis/glomerulonephritis)
4) Haemolytic anaemia (SLE, Vasculitis)

Glomerulonephritis can be categorised into rapidly progressive and slowly progressive. Give 3 examples of each

Rapidly progressive: Anti-GBM/Good pastures, ANCA vasculitis, Lupus nephritis, post-strep GN

Slowly progressive: IgA nephropathy (can become rapid), Membranoproliferative GN, Alport syndrome

Give 4 indications for a renal biopsy

What indications are present for those with a transplant kidney? Give 4

Original:
1) Dx of rapidly progressive GN
2) Nephrotic syndrome
3) SLE
4) AKI/CKD of unknown cause

Transplant:
1) Evaluation of acute kidney dysfunction
2) Any new or recurrent disease
3) After acute rejection (to assess response to therapy)
4) Protocol biopsy (conducted at specific time intervals post-transplant to detect subclinical rejection or other subclinical changes in high risk patients)

A patient having a solitary kidney is a contraindication for a kidney biopsy. What about in the case that it is a transplant patient?

If they are a transplant patient and one of the indications are met, then it is not contraindicated

Give 7 contraindications to performing a kidney biopsy

Solitary kidney (unless transplant)
Bleeding risk (high INR)
Pregnancy
Uncontrolled HTN
Active infection/sepsis
Bilateral small kidneys
Cystic kidney disease
Obstructed kidney
Anatomical abnormalities
Refusal of consent
Morbid obesity

Give 7 complications of performing a kidney biopsy

Bleeding risk
Infection (sepsis, site)
Failure
Iatrogenic damage to kidney and/or surrounding structures
AV fistula
Damage to adjacent organs
Loss of kidney
!!Perinephritic haematoma/abscess

Give 2 examples of nuclear medicine scans used in assessing renal disease and their primary use

DMSA scan for scarring
MAG3 scan for obstruction

When performing an US of the kidneys, how would you expect to find them in a case of AKI vs CKD

In AKI it is typically normal in size unless there is hydronephrosis or an obstruction

In CKD they are typically small and shrunken

when performing an US of kidneys in CKD, you would expect them to be small and shrunken. There are, however certain scenarios where it could appear large. Give 3

Diabetic nephropathy
Amyloidosis
Polycystic kidney disease

Compare and contrast between AKI and CKD based on the following investigations:
BUN:
Hb (Anaemia):
US:
PTH:
Ca:
K:
PO4:

AKI vs CKD
BUN: Raised vs normal
Hb (anaemia): Normal vs low (due to reduced EPO production)
US: Normal (except hydronephrosis) vs Small shrunken kidneys except
PTH: Normal vs raised (secondary hyperparathyroidism)
Ca: Normal (or low) vs Hypocalcaemia (secondary hyperparathyroidism due to reduced vit.D production + reduced PO4 excretion which means there is no negative feedback to PTH secretion)
K: both hyperkalaemia
PO4: Normal (unless severe) vs raised (reduced excretion)

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Nephrology Investigations Flashcards

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