Renal

Question 1

What is nephritic syndrome

Answer 1

Hypertension
Blood- Haematuria occurs due to podocytes developing large pores which allows blood and protein to escape into the urine.
Some protein
Fast onset
Low urine volume due to poor function

Question 2

What is nephrotic syndrome

Answer 2

Proteinuria >3.5g in 24hrs
Oedema
Hypoalbuminaemia
Hyperlipidaemia (by product of increased albumin production)

Question 3

Causes of nephritic syndrome

Answer 3

Post strep glomerulo nephitis

IgA Nephropathy

DM/ Vasculitis

Rapidly progressive glomerular nephritis

• Goodpastures
• Vasculitis - Wegner’s/ Churg strauss/ microscopic polyangitis

Question 4

Causes of nephrotic syndrome

Answer 4

Primary:
Minimal change
FSGS
Membranous glomerulonephitis

Secondary:
SLE

Hep B and C

HIV

Diabetes mellitus

Malignancy
Amyloidosis

Question 5

What is haemolytic uraemic syndrome

Answer 5

Triad of

Thrombocytopenia
Haemolytic Anaemia
AKI

Children
Emergency

Often after food poisoning/ gastroenteritis e.g. E coli, Shigella, Campylobacter

Question 6

What is minimal change glomerulonephritis

Answer 6

Nephrotic
• Childhood/ adolescence (commonest cause in children)
• Responds to steroids
• May recur
• Usually no progression to renal failure
• Loss of podocytes due to unknown circulating factor (not immune complex)

Question 7

What is FSGS

Answer 7

• Commonest in adults?
Other end of spectrum from minimal change
• Less responsive to steroids (need ciclosporin etc)
• Fibrosis/ scarring/ glomerulosclerosis
• Circulating factor causes – transplants often it recurs
• Progressive to renal failure
High recurrence in transplants

Question 8

What is Membranous glomerulonephritis?

Answer 8

• Causes kidney failure in a third of patients
• Immune complex deposits
• Autoimmune (likely) or secondary e.g. lymphoma, lupus or malaria.
• IgG

Question 9

What happens to kidneys in DM in context of nephrotic?

Answer 9

• Thickening of the basement membrane/ collagen
• Microvascular damage
• Mesangialsclerosis
• Progressive renal failure

Question 10

Describe IgA nephropathy

Answer 10

• Commonest GN
• Any age
• Haematuria can be invisible
• Mucosal infections relationship
• Variable histology and course
• Possible proteinuria
• Often renal failure
• Mesangial damage and scarring
• Immune complex deposition
• appears within a day or two after a URTI

Question 11

Describe hereditary nephropathies

Answer 11

•	Thin GBM nephropathy
•	Benign familial nephropathy
•	Isolated haematuria (blood is normal)
•	Alport:
X linked
Abormal collagen IV
Associated with deafness
Abnormal GBM
Progressive to renal failure

Question 12

What is Goodpastures?

Answer 12

• Uncommon
• Rapidly progressive
• Acute onset of severe nephritic syndrome
• Association with pulmonary haemorrhage (smokers)
• Autoantibody to collagen IV in BM
• Treatable by immune suppression and plasmaphoresis if caught early
(steroids and cyclophosphamide)
• IgG deposition with no Em deposit and inflam cells
Anti GBM

Question 13

Renin and aldosterone levels in Cushings Conns and Renal artery stenosis. Results?

Answer 13

Cushing’s and Conn’s would be associated with a high aldosterone and a low renin, renal artery stenosis would be associated with a high renin and aldosterone, Liddle’s (genetic) is associated with a low renin and aldosterone.

Hypertension and hypokalaemia

Question 14

Treatment hyperglycaemia

Answer 14

Manage precipitating factors, stop drugs e,g, ACEi

Stabilisation of the cardiac membrane
intravenous calcium gluconate by slow IV injection titrated to ECG response

Short-term shift in potassium from extracellular to intracellular fluid compartment
combined insulin/dextrose infusion
nebulised salbutamol
Consider NaHCo3 if acidotic

Removal of potassium from the body
calcium resonium (orally or enema)
loop diuretics
dialysis

Question 15

Cause and treatment of most common solid organ transplant recipiants

Answer 15

Cytomegalovirus

Ganciclovir

Question 16

Post-op complications of renal transplant

Answer 16

Post-op problems
ATN of graft
vascular thrombosis
urine leakage
UTI

Hyperacute acute rejection (minutes to hours)
due to pre-existent antibodies against donor HLA type 1 antigens (a type II hypersensitivity reaction)
rarely seen due to HLA matching

Acute graft failure (< 6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants

Causes of chronic graft failure (> 6 months)
both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)

Long term cancer - 25% have cancer after 20 years (often skin)

Question 17

ABG in sepsis

Answer 17

Patients who have sepsis often have a raised serum lactate due to the hypoperfusion of their peripheries. This gives them a metabolic acidosis with a raised anion gap.

Question 18

Raised anion gap vs normal?

Answer 18

If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids e.g.
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (diabetic ketoacidosis)
Drugs/ toxins (salicylates, methanol, ethylene glycol)

If there is a metabolic acidosis with a normal anion gap, then this is either due to loss of bicarbonate, or accumulation of H+ ions. Causes include:
Renal tubular acidosis
Diarrhoea
Addison's disease
Pancreatic fistula

Question 19

Management of acute renal colic

Answer 19

IM or oral Diclofenac
Alpha-adrenergic blockers to aid ureteric stone passage

US - 45% sensitivity
Non-contast CT if not

Lithotripsy or nephrolithotomy for severe cases. most pass within 4 weeks

<0.5cm then conservative

If assocaited infection then urgent need for decompression so percutaneous nephrostomy (in loin)

If large proximal stone (e.g. 2.3cm staghorn calculi) then pecutaneous nephrolithotomy as lipotrypsy has low clearence rate

Complex stone disease of CI of lithotripsy (preggers) then ureteroscopy

Question 20

Prevention of stones

Answer 20

Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet)
thiazides diuretics (increase distal tubular calcium resorption)

Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion

Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate

Question 21

factors which effect eGFR

Answer 21

pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being take

Question 22

eGRF variables

Answer 22

CAGE - Creatinine, Age, Gender, Ethnicity

Question 23

Complications in peritoneal dialysis

Answer 23

peritonitis: coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause
sclerosing peritonitis

Question 24

Way of diagnosing ATN

Answer 24

ATN rest the kidney, no fluid - one litre restriction. If you get brown cell card, fraction of Na in urine - More than 1% in urine = ATN.

Damage to tubular cells due to prolonged ischaemia or toxins
Kidneys can no longer concentrate urine or retain sodium - urine osmolality low, urine sodium high

Question 25

Staging of AKI

Answer 25

Stage Creatinine Urine production 1 Increase 1.5-1.9x baseline < 0.5ml/kg/h for >6 consecutive hours 2 Increase 2.0-2.9x baseline < 0.5ml/kg/h for >12 consecutive hours 3 Increase > 3x baseline or >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h 3 also is renal replacement therapy Only one thing needed

Question 26

Causes of transient or spurious non-visible haematuria

Answer 26

urinary tract infection menstruation vigorous exercise (this normally settles after around 3 days) sexual intercourse

Question 27

Causes of persistent non-visible haematuria

Answer 27

``` cancer (bladder, renal, prostate) stones benign prostatic hyperplasia prostatitis urethritis e.g. Chlamydia renal causes: IgA nephropathy, thin basement membrane disease ```

Question 28

Testing of haematuria

Answer 28

urine dipstick is the test of choice for detecting haematuria persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

Question 29

When to refer for haematuria for cancer screening

Answer 29

Urgent >45 and unexplain visible haematuria (no UTI Non-urgent Aged >60 with recurrent or persistent unexplained UTI

Question 30

What is Henoch- Schonlein purpura

Answer 30

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs abdominal pain polyarthritis features of IgA nephropathy may occur e.g. haematuria, renal failure analgesia for arthralgia treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants Self limiting

Question 31

Causes of hypokalaemia

Answer 31

1.) Increased potassium loss: Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics GI losses: diarrhoea, vomiting, ileostomy Renal causes: dialysis Endocrine disorders: hyperaldosteronism, Cushing's syndrome (OBVIOUSLY spirono is aldosterone antagonist) ``` 2.) Trans-cellular shift Insulin/glucose therapy Salbutamol Theophylline Metabolic alkalosis ``` 3. ) Decreased potassium intake 4. ) Magnesium depletion (associated with increased potassium loss)

Question 32

Treatment hypokalaemia

Answer 32

Mild to mod 2.5-3.4 = oral KI if asymptomatic and no ECG changed Severe hypokalaemia <2.5 or symptomatic = IV replacement, ITU/ cardiac monitoring. If no CI to fluiod therapy e.g. HF, then dilute to low concs to avoid plebitis. Don't exceed 20mmol/hr

Question 33

What is ADPKD

Answer 33

Aut dom polycystic kidney disease 1/1000 Caucasians Two loci PKD1 and 2 polycystin-1 and 2 Type 1 presents earlier US diagnosed based on age and number of cysts 2 or more and <60. 4 in both aged >60 Enlarged kidney

Question 34

How to tell DI?

Answer 34

Water suppression test - Stage 1 - no drink for 8 hours, measure weight and urine osmolality Stage 2 - Give Desmopressin (like ADH) if nephrogenic there will be no response

Question 35

Treatment of DI

Answer 35

``` Nephrogenic = Chlorothiazide Cranial = desmopressin (synthetic vasopressin) ```

Question 36

Features of chlamydia

Answer 36

asymptomatic in around 70% of women and 50% of men women: cervicitis (discharge, bleeding), dysuria men: urethral discharge, dysuria

Question 37

Symptoms of anaemia in CKD

Answer 37

Tachy Pale Aoritc flow murmur Predispsosition to LVH

Question 38

Causes of anaemia in renal failure

Answer 38

reduced erythropoietin levels - the most significant factor reduced erythropoiesis due to toxic effects of uraemia on bone marrow reduced absorption of iron anorexia/nausea due to uraemia reduced red cell survival (especially in haemodialysis) blood loss due to capillary fragility and poor platelet function stress ulceration leading to chronic blood loss

Question 39

How to calculate anion gap?

Answer 39

([Na+] + [K+]) - ([Cl] + [HCO3]) (how many anions extra) The anion gap is used to classify metabolic acidosis into either; Raised anion gap seen in e.g. diabetic ketoacidosis or, Normal anion gap seen in patients with diarrhoea due to gastrointestinal bicarbonate loss.

Question 40

Side effects of EPO

Answer 40

accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients) bone aches flu-like symptoms skin rashes, urticaria pure red cell aplasia* (due to antibodies against erythropoietin) raised PCV increases risk of thrombosis (e.g. Fistula) iron deficiency 2nd to increased erythropoiesis

Question 41

Diabetes inspidius is characterised by what biochem?

Answer 41

Diabetes insipidus is characterised by a high plasma osmolality and a low urine osmolality

Question 42

Signs of hypovolaemia

Answer 42

Low BP, tachy, poor tissue turgor (hand pinch), sunken eyes, dry mucous membranes, daily weight loss, low urine output, cap refil. Cap refil, BP, skin turgor are late chanes

Question 43

Signs of hypervolaemia

Answer 43

High BP, High JVP, weight gain, high urine output, lung crepitaions, periopheral oedema, gallop rhythm

Question 44

When to use colloid?

Answer 44

Blood for haemorrhage. HAS in speciallist use for hepatorenal syndrome

Question 45

Controversy regarding HCO3 in acidosis

Answer 45

Generate CO2 - adequate ventilation needed to prevent resp acidosis worsening NaHCO3 given so NA load and volume load which can cause fluid overload. Treat cause and in AKI may need RRT

Question 46

Possible indications for RRT in AKI

Answer 46

INdividual but suggestions: Persistent acidosis or hyperkalaemia Uraemia Fluid overload unresponsive

Question 47

Complications of RRT

Answer 47

``` Bleeding from anti coag Damage from catheter Drug accumulation/ clearence Altered nutrition Procedural hypotension ```

Question 48

Symptoms/ complications of AKI

Answer 48

``` Hyperkalaemia Hypertension Uraemia Pericarditis Acidosis Confusion Coma Fluid overload ```

Question 49

Pre renal causes AKI

Answer 49

``` Hypotension/ dehydration Vascular volume decrease e.g. haemorrhage CO decrease e.g. cardiogenicshocl, MI Peripheral vasodilation e.g. sepsis, drugs Renal artery stenosis Renal vasoconstriction NSAIDS, ACEi HRS ```

Question 50

Renal causes AKI

Answer 50

INterstitial Gentamicin, Cephalosporin, Lithium, Diuretics, pyelonephritis, infiltration e.g. sarcoid Glomerular disease e.g. FSGS Goodpastures, Glomerulonephritis, ATN (prolonged hypoperfusion) Vessels e.g. Vasculitis, Haemolytic uraemic syndrome, Thrombotic thrombocytopenic papura (autosomal recessive), DIC (due to cancers, trauma, sepsis, infection, allergy, aortic aneurisms)

Question 51

Post renal causes AKI

Answer 51

``` Ureteric stricture Renal calculi Transition cell Carcinoma Pelvic mass Iatrogenic ureter damage ```

Question 52

RFs AKI

Answer 52

``` CKD CVD Maligancy Age Male CliverD Complex surgery ```

Question 53

Initial management of AKI

Answer 53

``` NEWS >7 consider ITUK+ ECG - potassium Treat if >6.5 or ECG change Examine BP - fluid trial 500ml in 15min x 4 ```

Question 54

Monitoring of AKI

Answer 54

Catheter K+Obs every 4 hrs Lactate if signs of sepsis Daily creatine (24hr behind response)

Question 55

Investigations AKI

Answer 55

Urine dip ``` USS kidney LFTs (HRH) Thombocytopenia (if yes then bloodfilm for HUS) Intrinsic renal disease Igs Complement ANA ANCE Anti-GBM ```

Question 56

Supportative treatment AKI

Answer 56

Sepsis Stop nephrotoxic meds Stop drugs that may cause comps e.g. diuretics (K) metformin (acidosis), antihypertensives Check drug doses Gastroprotection and nutritional support Avoid contrast Consider referral e.g. stage 3

Question 57

More defiinitve treatment AKI

Answer 57

``` Refer to renal team if comps or stage 3 AKI Depends on cause Renal - biopsy and refer Post renal Catheter Nephrostomy Urological interventio Mange fluid balance, acidosis, hyperkalaemia ```

Question 58

Complications of nephrotic syndrome

Answer 58

Loss of AT3, C and S - rise in fibrogen predispose to thrombosis Los of Thyroxine binding globulin but not free thyroxine

Question 59

Signs and nsymptoms of polycystic kidney disease

Answer 59

``` HTY - RAAS overactivity Headache Haematuria Polyuria Back pain Cyst infections ```

Question 60

Treatment polycystic

Answer 60

Dietary restrictions | RRT

Question 61

What is diffuse proliferative glomerulonephritis?

Answer 61

classical post-streptococcal glomerulonephritis in child presents as nephritic syndrome / acute kidney injury most common form of renal disease in SLE

Question 62

What is clot retention??

Answer 62

Clot retention occurs as a sequal to bleeding in the urological tract. Large clots can become wedged in the urethra and cause acute urinary retention. It can be seen under any circumstance where there is macroscopic haematuria, but patients are most susceptible post operatively if bladder irrigation is not sufficient; they suffer from clot retention within the catheter. Treatment of the non operated patient is catheterisation with a three way catheter, with irrigation. In the post operative patient attempts should be made to mechanically free the clot.