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Phase 2a Sheffield Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What are the 6 nephrotic syndromes?

A
  • Diabetic nephropathy
  • Amyloidosis
  • Minimal change disease
  • Focal segmented glomerulosclerosis
  • Membranous neuropathy
  • Membranoproliferative glomerulonephritis
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2
Q

What is amylodiosis?

A

Amyloidosis refers to the disease state caused by abnormal amyloid protein deposits in organs.

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3
Q

What are the clinical manifestations of amyloidosis?

A
  • Kidney: swelling in the face, ankles, and legs
  • Heart: palpitations and shortness of breath
  • Intestines: malabsorption and weight loss
  • Large tongue: speech and swallowing difficulty, noisy breathing at night
  • Nerves: numbness or pain in the fingers and toes, alternating bouts of diarrhoea and constipation, orthostatic hypotension
  • CNS: Alzheimer’s memory loss and difficulty learning new things
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4
Q

What are the investigations for amyloidosis?

A
  • Fat pad biopsy: apple-green birefringence under polarised microscopy with Congo red stain.
  • SAP scan: to show amount and location of amyloid
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5
Q

What is the management for amyloidosis?

A
  • Organ transplant, if extensive damage.
  • AL amyloidosis:
    • Optimise nutrition, if malabsorption
    • Alkylating agent + corticosteroid: e.g. melphalan and prednisolone
    • Stem cell transplant
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6
Q

What is minimal change diease?

A

Minimal change disease (MCD) is a kidney disease that can cause nephrotic syndrome, a condition in which the kidneys leak large amounts of protein. It is called “minimal change” because the damage to the kidneys cannot be seen under a microscope.

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7
Q

What are the investigations for minimal change disease?

A
  • On light microscopy, the glomeruli look completely normal.
  • In some cases, there can be lipids in the proximal tubular cells.
  • Immunofluorescence is negative.
  • The only changes are seen on electron microscopy, where there’s effacement of podocyte foot processes.
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8
Q

What is the management for minimal change disease?

A

Idiopathic minimalchange disease is the only nephrotic disease that can be consistently treated with corticosteroids.

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9
Q

What is Focal Segmental Glomerulosclerosis?

A

Focal Segmental Glomerulosclerosis (FSGS) is a rare disease that affects the kidneys’ glomeruli, which are tiny blood vessels that filter waste and excess fluids from the blood. In FSGS, the glomeruli become scarred and damaged.

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10
Q

What are the investigations for Focal Segmental Glomerulosclerosis?

A
  • On light microscopy, there’s sclerosis and hyalinosis among the glomeruli.
  • FSG is segmental - only a part of the glomeruli is affected - and focal - only some of the glomeruli are affected.
  • Immunofluorescence is often negative, but can sometimes be positive for deposits of C3, C1 or IgM.
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11
Q

What is the management for Focal Segmental Glomerulosclerosis?

A

Primary FGS has an inconstant response to corticosteroids and some individuals may progress to CKD

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12
Q

What is Membranous Neuropathy?

A

Membranous neuropathy is a rare autoimmune disease that affects the nerves that control muscle movement and sensation in the body. It is also known as Membranous nephropathy or MN.

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13
Q

What are the clinical manifestations of membranous neuropathy?

A

The symptoms of membranous neuropathy can vary from person to person, but the most common symptoms include:
- Muscle weakness
- Tingling and numbness in the extremities
- Loss of reflexes
- Difficulty walking or standing
- Pain in the limbs
- Fatigue
- Loss of sensation in the limbs

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14
Q

What are the investigations for membranous neuropathy?

A

Biopsy
- Light microscopy - diffuse capillary and glomerular basement membrane thickening
- When the sample is stained with silver methenamine, irregular expansions can be seen
- Immunofluorescence will show that the immune complexes are granular and mostly made of IgG and C3.
- Electron microscopy
- flattening of the podocyte foot processes and sub-epithelial deposits of immune complexes.

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15
Q

What is the management for membranous neuropathy?

A

Poor response to corticosteroids and individuals may progress to CKD

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16
Q

What is Membranoproliferative Glomerulonephritis?

A

Three types of MPGN: they all cause proliferation of mesangial and endothelial cells in the glomerulus.

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17
Q

What are the risk factors for Membranoproliferative Glomerulonephritis?

A
  • Age (75% idiopathic)
  • Infections - hepatitis B, hepatitis C, HIV and endocarditis
  • Chronic lymphocytic leukaemiaand cryoglobulinaemia
  • Acquired partial lipodystrophy (ADP)
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18
Q

What are the signs of Membranoproliferative Glomerulonephritis?

A
  • Oedema
  • Oliguria
  • Haematuria
  • Hypertension
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19
Q

What are the symptoms of Membranoproliferative Glomerulonephritis?

A
  • Foamy urine (proteinuria)
  • Pink, red or ‘coke’ tinged urine (haematuria)
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20
Q

What are the investigations for Membranoproliferative Glomerulonephritis?

A
  • Urine dipstick
  • Urine microscopy and culture
  • U&Es
  • C3 and C4 levels
  • Renal biopsy for definitive diagnosis
    • PAS staining on light microscopywill show mesangial cell proliferation and capillary thickening
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21
Q

What is the management for Membranoproliferative Glomerulonephritis?

A

Primary MPGN
- Oral cyclophosphamide
- Oral mycophenolate mofetil (MMF) and oral corticosteroids

Secondary MPGN
- Treat the cause

General
- ACEi/ARB
- Statin
- Oral warfarin

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22
Q

What are the complications of Membranoproliferative Glomerulonephritis?

A
  • Hypertension
  • Infection susceptibility
  • Pro-thrombotic state
  • Hyeperlipidaemia
  • Hyperthyroidism
  • Hypocalcaemia
  • AKI
  • Chronic kidney disease
  • Rapidly progressive glomerulonephritis
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23
Q

What is post-streptococcal glomerulonephritis?

A

Post-streptococcal glomerulonephritis (PSGN) is usually an immunologically-mediated delayed consequence of pharyngitis or skin infections caused by streptococcus pyogenes.

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24
Q

What are the 8 nephritic syndromes?

A

– Post-streptococcal glomerulonephritis
- IgA neuropathy
- Good pastures syndrome
- SLE
- Diffuse proliferative glomerulonephritis
- Rapidly progressive glomerulonephritis
- Alport syndrome
- Membranoproliferative glomerulonephritis

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25
Q

What is a nephritic syndrome?

A

Nephritic syndrome is typically caused by inflammation that damages the glomerular basement membrane, leading to haematuria and red blood cell casts in the urine.

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26
Q

What is a nephrotic syndrome?

A

Nephrotic syndrome is defined as the presence of proteinuria, hypoalbuminaemia, and peripheral oedema.

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27
Q

What are the 5 features of a nephrotic syndrome?

A
  1. Proteinuria (> 3.5 g/day)
  2. Hypoalbuminemia (< 30 g/L) which leads tooedema
  3. Hyperlipidaemia as the liver increases synthesis of lipids in response to low albumin
  4. Hypogammaglobulinemia: due to loss of immunoglobulin in the urine
  5. Hypercoagulability: due to loss of antithrombin III, and protein C and S in the urine
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28
Q

What are the investigations for a nephrotic syndrome?

A
  • Urinalysis
  • 24-hour urine protein collection
  • Urine album: creatinine ratio
  • U&Es
  • LFTs
  • Lipid profile
  • Renal ultrasound
  • Renal biopsy
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29
Q

What are the clinical manifestations of a nephrotic syndrome?

A
  • Haematuria
  • Proteinuria
  • Arterial hypertension
  • Peripheral and peri-orbital oedema
  • Decreased urine output
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30
Q

What are the investigations for a nephritic syndrome?

A
  • Bloods
  • Urinalysis
  • Renal biopsy if needed
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31
Q

What are the clinical manifestations of post-streptococcal glomerulonephritis?

A
  • Haematuria
  • Signs of recent infection will be present
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32
Q

What are the investigations for post-streptococcal glomerulonephritis?

A
  • Bloods - low C3 and CH50.
  • Positive streptozyme test
  • Kidney biopsy
  • On light microscopy: the glomeruli are enlarged and hypercellular.
  • On immunofluorescence: IgG, IgM and C3 deposits along the glomerular basement membrane and the mesangium, which create a “starry sky” appearance.
  • On electron microscopy: subepithelial deposits which appear as “humps”.
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33
Q

What is the management for post-streptococcal glomerulonephritis?

A
  • Furosemide: for initial treatment of hypertension
  • Antibiotics
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34
Q

What is nephrolithiasis?

A

Renal stones, or nephrolithiasis, is the presence of stones, or calculi, within the urinary system.

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35
Q

What are the risk factors for kidney stones?

A
  • Gender → Male > Female
  • Dehydration
  • Previous kidney stone
  • Stone-forming foods: chocolate, rhubarb, spinach, tea, and most nuts are high in oxalate, and colas are high in phosphate
  • Genetic: cystinuria (Dent’s disease; cysteine stones), renal tubular acidosis (calcium phosphate stones)
  • Systemic disease: Crohn’s disease (calcium oxalate stones)
  • Metabolic:hypercalcaemia, hyperparathyroidism, hypercalciuria (calcium stones)
  • Kidney disease-related: medullary sponge kidney, AD polycystic kidney disease
  • Anatomical abnormalities that predispose to stone formation e.g. duplex,
    obstruction or trauma
  • Drugs: loop diuretics and acetazolamide can cause calcium stones; protease inhibitors (HIV medication) cause radiolucent stones
  • Exposure: cadmium or beryllium
  • Other: gout and ileostomies (uric acid stones)
  • Family history
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36
Q

What are the signs of kidney stones?

A
  • Flank or renal-angle tenderness
  • Fever
  • Hypotension and tachycardia: may indicate urosepsis / a septic stone
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37
Q

What are the symptoms of kidney stones?

A
  • Acute, severe flank pain (renal colic)
    • Classically ‘loin to groin’ pain
    • Pain lasts minutes to hours and occurs in spasms (with intervals of no pain or dull ache)
    • Fluctuating in severity as the stone moves and settles
  • Nausea and vomiting
  • Urinary urgency or frequency
  • Haematuria: microsopic or macroscopic
  • May present with oliguria
  • Fever: suggests a septic stone or pyelonephritis
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38
Q

What are the investigations for kidney stones?

A
  • GOLD STANDARD - Non-contrast CT KUB
  • Urinalysis
  • Inflammatory markers:elevated WBCs and CRP
  • U&Es
  • Bone profile and urate
  • FBC
  • Urine dipstick
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39
Q

What are the differential diagnoses for kidney stones?

A
  • Ruptured abdominal aortic aneurysm
  • Appendicitis
  • Ectopic pregnancy
  • Ovarian cyst
  • Bowel obstruction
  • Diverticulitis
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40
Q

What is the acute management for kidney stones?

A
  • IV fluids and anti-emetics
  • Analgesia: an NSAID by any route is considered first-line
  • Antibiotics if infection is present
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41
Q

What is the conservative management for kidney stones?

A
  • Watchful waiting: stones <5mm should pass spontaneously and followed up in clinic
  • Medical expulsive therapy (MET):Alpha-blocker, e.g.tamsulosin, for ureteric stones 5-10mm to help passage. Not indicated for renal stones.
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42
Q

What are the surgical options for kidney stones?

A
  • Ureteroscopy
  • Extracorporeal shock wave lithotripsy (ESWL)
  • Percutaneous nephrolithotomy (PCNL)
  • Ureteral stenting
  • Percutaneous nephrostomy
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43
Q

What is the patient advice for recurrent kidney stones?

A
  • Increase oral fluids
  • Reduce dietary salt intake
  • Reduce intake of oxalate-rich foods for calcium stones (e.g. spinach, nuts, rhubarb, tea)
  • Reduce intake of urate- rich foods for uric acid stones (e.g. kidney, liver, sardines)
  • Limit dietary protein
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44
Q

What are the complications of kidney stones?

A
  • Obstruction and hydronephrosis: acute kidney injury and renal failure
  • Urosepsis: an infected, obstructing stone is a urological emergency and requires urgent decompression
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45
Q

What is acute pyelonephritis?

A

Upper urinary tract infection: acute inflammation of the renal pelvis (join between kidney and ureter) and parenchyma.

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46
Q

What are the risk factors for acute pyelonephritis?

A
  • Vesico-ureteral reflux (VUR)
  • Gender → Female
  • Sexual intercourse
  • Indwelling catheter
  • Diabetes mellitus
  • Pregnancy
  • Urinary tract obstruction e.g. calculi (stones)
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47
Q

What are the signs of acute pyelonephritis?

A
  • Tender loin on examination
  • Pain on bimanual palpation of the renal angle (over kidney)
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48
Q

What are the symptoms of acute pyelonephritis?

A
  • High fever and rigors
  • Loin to groin pain
  • Dysuria and urinary frequency
  • Haematuria
  • Other non-specific symptoms (e.g. nausea and vomiting)
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49
Q

What are the investigations of acute pyelonephritis?

A
  • GOLD STANDARD - Mid-stream urine MCS
  • Urine dipstick - FIRST LINE
  • Bloods
  • CRP and ESR
  • CT can help confirm diagnosis
  • DMSA scan
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50
Q

What are the differential diagnoses of acute pyelonephritis?

A
  • Lower UTI
  • Cystitis
  • Acute prostatitis
  • Urethritis
  • Chronic pyelonephritis
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51
Q

What is the management for acute pyelonephritis?

A

First line
- Broad spectrum antibiotics (e.g. co-amoxiclav) until culture and sensitivities are available
- Hydration

Other
- - IV rehydration
- Analgesia
- Antipyretics
- Surgery to drain abscesses or relieve calculi that are causing infection

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52
Q

What are the complications of acute pyelonephritis?

A
  • Renal abscess
  • Recurrent infections
    • Chronic pyelonephritis
    • Papillary necrosis
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53
Q

What is chronic pyelonphritis?

A

Upper urinary tract infection: chronic inflammation of the renal pelvis (join between kidney and ureter) and parenchyma.

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54
Q

What are the risk factors for chronic pyelonephritis?

A
  • Vesico-ureteral reflux
  • Chronic obstruction
    • Kidney stones
    • Congenital malformations e.g. of the posterior urethral valve
    • BPH
    • Cervical carcinoma
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55
Q

What are the signs of chronic pyelonephritis?

A
  • Tender loin on examination
  • Pain on bimanual palpation of the renal angle (over kidney)
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56
Q

What are the symptoms of chronic pyelonephritis?

A
  • High fever and rigors
  • Loin to groin pain
  • Dysuria and urinary frequency
  • Haematuria
  • Other non-specific symptoms (e.g. nausea and vomiting)
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57
Q

What are the investigations of chronic pyelonephritis?

A
  • GOLD STANDARD - Mid-stream urine MCS
  • Urine dipstick - FIRST LINE
  • Bloods
  • CRP and ESR
  • CT can help confirm diagnosis
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58
Q

What are the differential diagnoses for chronic pyelonephritis?

A
  • Lower UTI
  • Cystitis
  • Acute prostatitis
  • Urethritis
  • Acute pyelonephritis
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59
Q

What is the management for chronic pyelonephritis?

A
  • Correct the underlying cause of recurrent infection e.g. surgery to correct congenital structural causes or to remove obstruction like kidney stones
  • Dialysis may be needed
  • Nephrectomy might be needed.
  • Antibiotics may play a role
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60
Q

What are the complications of chronic pyelonephritis?

A
  • Renal abscess
  • Acute renal failure
  • Chronic kidney disease
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61
Q

What is chronic kidney disease?

A

Chronic kidney disease (CKD) describes a progressive deterioration in renal function. These issues develop over at least 3 months.

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62
Q

What are the risk factors for chronic kidney disease?

A
  • Increasing age
  • Afro-Caribbean
  • Diabetes mellitus
  • Hypertension
  • Autoimmune conditions
  • Glomerulonephritis
  • Congenital abnormalities
  • Nephrotoxic drugs
  • Smoking
  • Enlarged prostate
  • Renal artery stenosis
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63
Q

What are the signs for chronic kidney disease?

A
  • Hypertension
  • Fluid overload
  • Uraemic sallow: a yellow or pale brown colour of skin
  • Uraemic frost: urea crystals can deposit in the skin
  • Pallor: due to anaemia
  • Evidence of underlying cause: e.g. butterfly rash in lupus
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64
Q

What are the symptoms of chronic kidney disease?

A
  • Lethargy
  • Pruritis
  • Muscle cramps
  • Nausea
  • Anorexia
  • Loss of appetite
  • Frothy urine
  • Swollen ankles/ oedema
  • Increased bleeding: excess urea in the blood makes platelets less likely to stick to each other
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65
Q

What are the investigations for chronic kidney disease?

A
  • Urine dip stick test
  • Urine albumin: creatinine ratio
  • U&Es
  • FBC
  • Bone profile and PTH
  • Renal ultrasound

Consider
- CT KUB
- Renal biopsy
- Investigate the underlying cause

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66
Q

What is the management of chronic kidney disease?

A
  • Lifestyle changes
  • Cause related management
  • Renal replacement therapy e.g. dialysis when eGFR is in single digits
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67
Q

What are the complications of chronic kidney disease?

A
  • Cardiovascular
  • CDK-mineral bone disease
  • Anaemia
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68
Q

What is cystitis?

A

Lower urinary tract infection: inflammation of the bladder.

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69
Q

What are the risk factors for cystitis?

A
  • Female
  • Post-menopause
  • Sexual intercourse
  • Diabetes
  • Catheterisation
  • Urinary stasis
  • ## Risk factors for UTIs
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70
Q

What are the clinical manifestations of cystitis?

A

Signs
- Suprapubic tenderness

Symptoms
- Dysuria
- Increasing urine frequency
- Urgency to urinate
- Nocturia
- Changes in urine appearance

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71
Q

What are the investigations for cystitis?

A
  • Urine dipstick: nitrite and leukocyte usually positive
  • GOLD STANDARD - Mid-stream urine microscopy, culture and sensitivity (MC&S)

Other
- Bladder scan
- Renal tract ultrasound
- Cystocopy
- DMSA
- Micturating Cystourethrogram

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72
Q

What are the differential diagnoses of cystitis?

A
  • Pyelonephritis.
  • Urethritis
  • Serious illness e.g. sepsis should be considered in the presence ofred flagssuch as loin pain, rigors, nausea, vomiting, and altered mental state
73
Q

What is the management for cystitis in men?

A
  • First line: Antibiotic course for 7 days - trimethoprim or nitrofurantoin
  • Second line: Antibiotic course for 7 days - amoxicillin or cefalexin
  • Consider urological cancer referral if suspected e.g. if persistent UTI, haematuria, dysuria, raised WBC
74
Q

What is the management for cystitis in non-pregnant women?

A
  • If symptoms are mild, antibiotics may be delayed
  • First line: Antibiotic course for 3 days - nitrofurantoin or trimethoprim
  • Second line: Antibiotic course for 3 days - nitrofurantoin or pivmecillinam or fosfomycin single-dose sachet
75
Q

What is the management for cystitis in pregnant women?

A
  • First line: Antibiotic course for 7 days - nitrofurantoin
  • Second line: Antibiotic course for 7 days - amoxicillin or cefalexin
76
Q

What is the management for cystitis in catheterised women

A
  • First-line: nitrofurantoin or trimethoprim for7 days
  • Check forblockageandconsider changingthe catheter if it has been in place formore than 7 days
77
Q

What are the complications of cystitis?

A
  • Pyelonephritis
  • Renalandperi-renal abscess
  • Impaired renal function orrenalfailure
  • Urosepsis
  • Prostatitis
  • Urinary stones
78
Q

What is Urethritis?

A

Urethral inflammation due to infectious or non-infectious causes. It is primarily a sexually acquired disease.

79
Q

What are the risk factors for urethritis?

A
  • Sexually active
  • Multiple sexual partners
  • Unprotected sex
  • Male to male sex
  • Male
80
Q

What are the clinical manifestations of urethritis?

A
  • May be asymptomatic (90-95% with gonorrhoea, 50% of patients with chlamydia)
  • Dysuria (painful urination) +/- discharge; blood or pus
  • Urethral pruritus
  • Urethral pain
  • Penile discomfort
  • Inflammation/ oedema
  • Skin lesions
  • Systemic symptoms
81
Q

What are the differential diagnoses for urethritis?

A
  • UTI
  • Candida balanitis or vaginitis
  • Epididymitis
  • Interstitial cystitis
  • Chronic prostatitis
  • Urethral malignancy
  • Nephrolithiasis
82
Q

What are the complications for urethritis?

A
  • Reactive arthritis
  • Gonococcal conjunctivitis
  • Periurethral abscess
  • Urethral stricture or fistula
  • Epididymitis
  • Prostatitis
  • Penile lymphangitis
83
Q

What are the investigations for urethritis?

A
  • Nucleic acid amplification test (NAAT):
    • Female - self collected vaginal swab (best), endocervical swab, first void
      urine
    • Male - first void volume
    • High specificity and sensitivity
  • Microscopy of gram-stained smears of genital secretions
  • Blood cultures
  • Urine dipstick - to exclude UTI
  • Urethral smear
84
Q

What is the management for urethritis?

A
  • Chlamydia:
    • Oral azithromycin or oral doxycycline
    • Tests for other STIs
    • If pregnant:
      • Oral erythromycin or oral azithromycin
  • Gonorrhoea:
    • IM ceftriaxone with oral azithromycin
  • Partner notification
  • Patient education
  • Contact tracing
85
Q

What is autosomal dominant polycystic kidney disease?

A

Autosomal dominant polycystic kidney disease is a common genetic disorder characterised by multiple renal cysts.

86
Q

What are the risk factors for autosomal dominant polycystic kidney disease?

A
  • PKD1 mutation
  • Afro-Caribbean ancestry
  • Hypertension
  • Male gender
87
Q

What are the signs of autosomal dominant polycystic kidney disease?

A
  • Bilateral flank masses: due to large polycystic kidneys
  • Hypertension: seen in most patients by 4th decade of life
88
Q

What are the symptoms of autosomal dominant polycystic kidney disease?

A
  • Abdominal, flank or back pain: due to large size or cyst complications (rupture/infection)
  • Haematuria
  • Dysuria and fever
  • Renal colic
  • Constitutional features of chronic kidney disease: fatigue, weakness, reduced energy
  • Polyuria, polydipsia, nocturia
89
Q

What are the extra-renal manifestations of autosomal dominant polycystic kidney disease?

A
  • Polycystic liver disease: seen in > 80% of patients on MRI imaging.
  • Pancreatic cysts
  • Cerebral aneurysms
  • Cardiac valve disease
  • Gastrointestinal abnormalities
  • Seminal vesicle cysts and infertility
90
Q

What are the investigations for autosomal dominant polycystic kidney disease?

A
  • Imaging:
    • FIRST LINE - Ultrasound: principle investigations, especially in screening
    • Renal MRI/CT: high sensitivity and good for assessing progression (e.g. kidney size). Useful if concern regarding renal cell carcinoma (RCC)
    • CT KUB: if presenting with suspected renal stone
    • Cerebral imaging (e.g. MRA): screening for cerebral aneurysms
91
Q

What is the ultrasound diagnostic criteria for autosomal dominant polycystic kidney disease?

A
  • If positive family history
    • < 30 years: ≥3 cysts (unilateral or bilateral)
    • 30-39 years: ≥3 cysts (unilateral or bilateral)
    • 40-59 years: ≥2 cysts in each kidney
  • If no family history is present, there isno established imaging based criteria. Generally, a diagnosis can be made in the presence of multiple bilateral renal cysts (e.g. ≥10 and ≥5mm in size) or bilateral renal enlargement with cysts.
  • MRI/CT of abdomen or pelvis
  • Urinalysis
92
Q

What are the differential diagnoses for autosomal dominant polycystic kidney disease?

A
  • Multiple benign cysts
  • Localised cystic benign: unilateral disease
  • Acquired renal cystic disease: may be seen in patients with CKD on dialysis
  • Medullary sponge kidney: congenital disorder of collecting ducts and calyceal system
  • Other genetic conditions: e.g. autosomal recessive polycystic kidney disease, tuberous sclerosis
93
Q

What is the management for autosomal dominant polycystic kidney disease?

A

Management is used to target symptoms:

  • Blood pressure control: ACEi e.g. Enalapril
  • Vasopressin receptor agonist: Tolvaptan
  • UTI: antibiotics
  • Analgesia for pain
  • Dialysis or transplant
  • Genetic counselling
  • Regular ultrasound to monitor cysts
94
Q

What are the complications of autosomal dominant polycystic kidney disease?

A
  • Ruptured cyst
  • Haemorrhagic cyst
  • Infected cyst: many occur in relation to rupture.Typical features include fever, pain, dysuria.
  • Renal stones
  • Hypertension
  • ESRD
  • Sepsis
  • Cerebral haemorrhage(e.g. aneurysm rupture)
  • Progressive liver disease: if cystic liver
  • Cardiovascular disease
95
Q

What is autosomal recessive polycystic kidney disease?

A
  • Autosomal recessive condition in which the kidneys become filled with hundreds of fluid-filled sacs, causing them to be larger than normal and to quit functioning over time.
  • ARPKD is rarer and more severe than ADPKD.
96
Q

What are the risk factors for autosomal recessive polycystic kidney disease?

A

Family History

97
Q

What are the clinical manifestations of autosomal recessive polycystic kidney disease?

A
  • Oligohydramnios,pulmonary hypoplasiaandPotter syndrome
  • Cystic enlargementof therenalcollecting ducts
  • May present with renal failure at birth
  • Congenital liver fibrosis
98
Q

What are the investigations for autosomal recessive polycystic kidney disease?

A
  • Prenatal ultrasound: may show bilaterally large kidneys with cysts and oligohydramnios
  • OR neonatal ultrasound
  • CT & MRI: to monitor liver disease
  • Genetic testing
99
Q

What are the differential diagnoses for autosomal recessive polycystic kidney disease?

A
  • ADPKD
  • Acquired cystic kidney disease
  • Benign cysts
  • Tuberous sclerosis
  • Multi-cystic dysplasia: one kidney only is made up of cysts. Other kidney is normal
  • Medullary sponge kidney: congenital disorder of collecting ducts and calyceal system
  • Hydro-nephrosis
  • Renal vein thrombosis
100
Q

What is the management for autosomal recessive polycystic kidney disease?

A

No actual treatment. Management of PKD is usually directed at specific symptoms and organ dysfunction.

  • Hypertension: treated with ACE inhibitors
  • Analgesia for renal colic related to stones or cysts. (Not NSAIDs)
  • Antibiotics for infection. Drainage of infected cysts may be required.
  • In cases of kidney failure, dialysis or kidney transplant are sometimes needed. Patients may require dialysis in first few days of life with ARPKD
  • Genetic counselling for family members
101
Q

What are the complications for autosomal recessive polycystic kidney disease?

A
  • Liver failuredue to liver fibrosis
  • Portal hypertensionleading to oesophageal varices and other complications
  • Progressive renal failure
  • Hypertensiondue to renal failure
  • Chronic lung disease
102
Q

Define urinary incontinence?

A

Urinary incontinence is a problem where the process of urination, also called micturition, happens involuntarily.

103
Q

What are the risk factors for urinary incontinence?

A
  • Increased age
  • Postmenopausal status
  • Obesity
  • Pregnancy
  • Vaginal delivery
  • Prostate surgery
  • Pelvic floor surgery
  • Pelvic organ prolapse
  • Neurological conditions, such as multiple sclerosis
  • Cognitive impairment and dementia
104
Q

What are the clinical manifestations of urinary incontinence?

A
  • Urge incontinence: frequent urination, especially at night
  • Stress incontinence: urinary leakage with pressure applied to the abdomen
  • Overflow incontinence: weak or intermittent stream or hesitancy
105
Q

What should be asked in the history regarding urinary incontinence?

A
  • A medical history should distinguish between the types of incontinence.
  • Assess for modifiable risk factors:
    • Caffeine consumption
    • Alcohol consumption
    • Medications
    • Body mass index (BMI)
  • Assess theseverityby asking about:
    • Frequency of urination
    • Frequency of incontinence
    • Nighttime urination
    • Use of pads and changes of clothing
106
Q

What investigations should be done for urinary incontinence?

A
  • Examinationshould assess thepelvic toneand examine for:
    • Pelvic organ prolapse
    • Atrophic vaginitis
    • Urethral diverticulum
    • Pelvic masses
  • Bladder diary
  • Urine dipstick
  • post-void residual volume
  • Urodynamics
107
Q

What is the RUSHES mnemonic for LUTS?

A

Indications for surgery for LUTS mnemonic

RUSHES

- R -  Retention
- U - UTI’s
- S - Stones
- H - Haematuria
- E - Elevated creatinine due to bladder outflow obstruction
- S - Symptoms deterioration
108
Q

What are the 4 types of non-urothelial bladder cancers?

A
  • Squamous cell carcinoma (1-7%)
  • Adenocarcinoma (2%)
  • Sarcoma (>1%)
  • Small cell (>1%)
109
Q

What is transitional cell carcinoma?

A

Transitional epithelium lines the renal pelvis, ureter, bladder, and urethra. Transitional cell carcinoma (TCC) most typically arises within the bladder.

110
Q

What are the risk factors for transitional cell carcinoma?

A
  • Increasing age: most common in patients aged 50 to 80 years old
  • Gender → Male > Female
  • Family history
  • Alcohol
  • Extended dwell times: not emptying bladder for long periods of time
  • Carcinogens: mnemonic PeeSAC
    • Phenacetin - an old analgesic
    • Smoking
    • Alanine - rubber, dye and textile industries
    • Cyclophosphamide: medication used to treat cancers and autoimmune diseases
  • Occupational exposure
111
Q

What are the signs of transitional cell carcinoma?

A
  • Palpable suprapubic mass in advanced cases
  • Anaemia e.g. pallor, if chronic bleeding present
112
Q

What are the symptoms of transitional cell carcinoma?

A
  • ‘Painless’ haematuria: microscopic or macroscopic
  • Dysuria (pain when urinating) can occur
  • Frequency
  • Constitutional symptoms e.g. weight loss
113
Q

What are the NICE guidelines regarding transitional cell carcinoma referral?

A

As per NICE guidelines, refer people for an appointment within 2 weeks if they are:

  • Aged 45 and overand have:
    • Unexplained visible haematuriawithouturinary tract infection,OR
    • Visible haematuria that persists or recursaftersuccessful treatment of urinary tract infection,OR
  • Aged 60 and overand have: unexplained microscopic haematuriaandeither dysuriaora raised WCC on a blood test
  • Considernon-urgent referral for bladder cancer in peopleaged 60 and overwith recurrent or persistent unexplained urinary tract infections.
114
Q

What are the investigations for transitional cell carcinoma?

A
  • FIRST LINE - Urinalysis
  • FBC
  • U&Es
  • Bone profile
  • LFTs and coagulation scores
  • Urinary cytology
  • Flexible cystoscopy

Investigations for staging
- CT (CTAP and CT urogram)
- Pelvic MRI
- PET CT
- Bone scan

115
Q

What staging system is used for bladder cancer?

A

TNM

116
Q

What is the management for superficial transitional cell carcinoma?

A
  • Trans-urethral resection of bladder tumour (TURBT): rigid cystoscopy under general anaesthetic, with a post-operative dose of intravesical mitomycin C (chemotherapy). Further management will depend on the risk as determined by histology
    • Low risk:no further management
    • Intermediate risk:6 doses of intravesical mitomycin C
    • High risk:intravesical BCG vaccine, or radical cystectomy if very high risk
117
Q

What is the management for muscle invasive transitional cell carcinoma?

A
  • Radical cystectomywith neoadjuvant chemotherapy; patients will require an ileal conduit (urostomy)
  • Radical radiotherapywith neoadjuvant chemotherapy is an alternative to surgery
118
Q

What is the management for locally-advanced or metastatic transitional cell carcinoma?

A
  • Chemotherapy:cisplatin-based chemotherapy is generally offered
  • Palliative treatment: e.g. radiotherapy for bladder symptoms if curative treatment is not an option
119
Q

What are the complications of transitional cell carcinoma?

A
  • Obstructive uropathy:bladder outflow obstruction causing urinary retention
  • Metastasis:bone, lung and liver are most common
120
Q

What are non-urothelial bladder cancers?

A
  • Non-urothelial bladder cancers are a group of rare cancers that arise from tissues in the bladder other than the urothelium.
  • These cancers can include squamous cell carcinoma, adenocarcinoma, and small cell carcinoma.
  • Non-urothelial bladder cancers make up a small percentage of all bladder cancers and are often more aggressive and harder to treat than urothelial bladder cancers.
121
Q

What is AKI?

A
  • Acute kidney injury (AKI) is defined as a sudden decline in renal function over hours or days.
  • A decline in renal function can lead to dysregulation of fluid balance, acid-base homeostasis and electrolytes.
122
Q

What is the RIFLE mnemonic for AKI?

A
  • RIFLE describes three levels of renal dysfunction (RIF) and two outcome
    measures (LE) - these criteria indicate an increasing degree of renal damage
    and have a predictive value for mortality
  • Criteria:
    • Risk
    • Injury
    • Failure
    • Loss
    • End-stage renal disease
123
Q

What are the risk factors for AKI?

A
  • Age(> 65 years old)
  • History of AKI
  • CKD
  • Poor fluid intake/ increased loss
  • Urological historye.g. stones
  • Cardiac failure
  • Peripheral vascular disease
  • Diabetes mellitus
  • Sepsis
  • Hypovolaemia
  • Nephrotoxic drug use e.g. NSAIDS and ACE inhibitors
  • Liver disease
  • Cognitive impairment
  • Contrast agents e.g. during CT
124
Q

What are the pre-renal symptoms of AKI that are due to hypovolaemia?

A
  • Reduced capillary refill time
  • Dry mucous membranes
  • Reduced skin turgor
  • Cool extremities
  • Thirst
  • Reduced urine output
  • Dizziness
  • Confusion: in elderly patients
  • Signs of fluid loss: excessive sweating, vomiting, diarrhoea and polyuria
  • Orthostatic hypotension
  • Tachycardia
125
Q

What are the post-renal signs of AKI that are due to hypervolemia?

A
  • Ankle swelling
  • Orthopnoea: sensation of breathlessness in lying down position
  • Paroxysmal nocturnal dyspnoea
  • Dyspnoea
  • Raised JVP
  • Ascites
126
Q

What are the intra-renal signs of AKI?

A
  • Vascular: arterial hypertension; peripheral oedema
  • Nephrotic syndrome: heavy proteinuria; hypoalbuminaemia and oedema
  • Nephritic syndrome: haematuria; proteinuria; oliguria and hypertension
  • Tubulo-interstitial disease: arthralgia, rashes and fever
127
Q

What are the post-renal sings of AKI?

A
  • Urinary stones: loin-to-groin pain, haematuria, nausea and vomiting.
  • Prostatic issues: dysuria, frequency, terminal dribbling, hesitancy
  • Obstruction at the bladder neck: may be associated with a palpable bladder and a tender suprapubic area.
128
Q

What are the investigations for AKI?

A
  • Assess the current fluid state.
  • Review of medical chart
  • Urinalysis
  • FBC
  • U&E
  • ABG
  • Creatine kinase
  • Clotting
  • Blood film
  • Complement
  • Immunoglobulins
  • Serum electrophoresis
  • Virology(hepatitis B/C)
  • Imaging
129
Q

What are the complications of AKI?

A
  • Hyperkalaemia: when the individual is oliguric, potassium isn’t effectively removed from the blood.
  • Fluid overload
  • Metabolic acidosis
  • Uraemia
    • Uraemic complications: e.g. encephalopathy, pericarditis
130
Q

What is renal cell carcinoma?

A
  • Renal cell carcinoma (RCC) is an adenocarcinoma most commonly arising from the epithelium of the proximal convoluted tubule.
  • It is also known as hypernephroma or Grawitz tumour
131
Q

What are the risk factors for renal cell carcinoma?

A
  • Increasing age: peak age between 60 and 70 years of age
  • Male: 3:2 ratio of men to women
  • Black ethnicity
  • Hereditarye.g. Von Hippel-Lindau
  • Smoking
  • Obesity
  • Hypertension
  • Haemodialysis
132
Q

What are the signs of renal cell carcinoma?

A
  • Hypertension: risk factor
  • Flank mass
  • Left-sided varicocele
    • Left testicular vein drains into the left renal vein; a left RCC can invade the renal vein causing back-pressure and varicocele formation in left testes
    • Right testicular vein drainsdirectlyinto the IVC, therefore a right RCC doesnotcause a varicocele
  • Evidence of metastatic disease
    • SOB
    • Chronic liver disease
    • Bone pain
133
Q

What are the symptoms of renal cell carcinoma?

A
  • Asymptomatic: over 50% of cases are diagnosed incidentally
  • Classic triad: haematuria, flank pain, abdominal mass (seen in 10-15% of patients)
  • Constitutional symptoms: e.g. weight loss, fatigue, fever of unknown origin
  • 25% of patients have metastatic disease at presentation.
134
Q

What are the investigations for renal cell carcinoma?

A
  • CT is GOLD STANDARD
  • Urinalysis
  • Bloods
    • FBC
    • U&Es
    • LFTs
    • Bone profile
    • LDH
  • Abdominal ultrasound
  • Needle biopsy
135
Q

What staging system does renal cell carcinoma use?

A

TNM

136
Q

What is the management for localised renal cell carcinoma?

A
  • Partial nephrectomy:standard for T1 tumours (i.e. ≤ 7cm) and performed with curative intent
  • Radical nephrectomy: standard for T2-T4 tumours (i.e. > 7cm). Local lymph node dissection and adrenalectomy may be considered if these structures are involved
  • Minimally-invasive procedures: reserved for patients unfit for surgery, e.g. radiofrequency ablation or embolisation
137
Q

What is the management for metastatic renal cell carcinoma?

A
  • Molecular therapy:Sunitinib and Pazopanib (receptor tyrosine kinase inhibitors) are FIRST LINE agents
  • Radiotherapy: some patients are suitable for palliative radiotherapy
  • Cytoreductive surgery: some patients are suitable for a debulking, non-curative nephrectomy as there is evidence for a slight improvement in survival
138
Q

What are the complications of renal cell carcinoma?

A
  • Metastasis:adrenal, liver, bone, lung, brain
    • Metastases to lung is common: cannon ball metastases
  • Paraneoplastic syndromes
    • Erythropoietin -> polycythaemia
    • PTH -> hypercalcaemia
    • ACTH -> Raises cortisol levels and causes Cushing’s syndrome
    • Renin -> affects blood pressure
  • Stauffer syndrome: also known as paraneoplastic nephrogenic hepatomegaly
139
Q

What is nephroblastoma?

A
  • Also known as Wilms tumour
  • Wilms’ tumour is a specific type of tumour affecting the kidney in children, typically under the age of 5 years.
140
Q

What are the risk factors for nephroblastoma?

A
  • Family history
  • Congenital syndromes: Wilms’ tumour presents as part of some syndromes e.g. WAGR, Denys-Drash, Beckwith-Wiedemann syndromes and hemihypertrophy
141
Q

What are the signs of nephroblastoma?

A
  • Abdominal mass
  • Microscopic haematuria
  • Hypertension
142
Q

What are the symptoms of nephroblastoma?

A
  • Abdominal/ flank pain
  • Haematuria
  • Lethargy
  • Fever
  • Weight loss
  • Hypertension
143
Q

What are the investigations for nephroblastoma?

A
  • Urinalysis
  • U&Es
  • Ultrasound of the abdomen
  • CT or MRI for staging
  • Biopsy required to make a definitive diagnosis
144
Q

What is the management for nephroblastoma?

A
  • Surgical excisionof the tumour along with the affected kidney (nephrectomy).
  • Adjuvant chemotherapy
  • Adjuvant radiotherapy
  • Renal transplantation: usually reserved for patients with advanced, bilateral disease and renal failure
145
Q

What are the complications of nephroblastoma?

A
  • Renal failure:rare but occasionally seen in those with bilateral disease
  • Chemotherapy-related complications: such as bone marrow suppression and neutropenic sepsis
146
Q

What is IgA neuropathy?

A
  • IgA nephropathy (IgAN) is defined by the presence of dominant or co-dominant mesangial IgA immune deposits, often accompanied by C3 and IgG in association with a mesangial proliferative glomerulonephritis of varying severity.
  • Formerly called Berger’s disease.
147
Q

What are the risk factors for IgA neuropathy?

A
  • Adolescents and middle age
  • Male gender
  • Ethnicity: IgA nephropathy is more common in Asian populations than Caucasian populations
  • Preceding URTI or gastroenteritis
  • HIV
  • Family history: an autosomal dominant familial form of IgA nephropathy exists
  • Presence of other autoimmune conditions: linked to conditions such as HSP, SLE, coeliac diseaseand alcoholic liver disease
148
Q

What are the signs of IgA neuropathy?

A
  • Haematuria
    • Macroscopic: particularly in younger patients
    • Microscopic: particularly in older patients
  • Oedema: due to proteinuria
  • Cervical lymphadenopathy: suggests an URTI as a recent trigger
  • Hypertension
149
Q

What are the symptoms of IgA neuropathy?

A
  • Pink, red or “coke” tinged urine (haematuria)
  • Foamy urine (proteinuria)
  • Sore throat: suggests an URTI as a recent trigger
  • Loose stools and abdominal discomfort: suggests gastroenteritis as a recent trigger
150
Q

What are the investigations for IgA neuropathy?

A
  • Renal biopsy - GOLD STANDARD - required to make diagnosis
  • Urinalysis
  • Urine microscopy and culture
  • C3/C4 complements
  • Urine dipstick
  • U&Es
151
Q

What is the differential diagnosis of IgA neuropathy?

A

IgA vasculitis, also known as Henoch-Schonlein purpura: the difference is IgA nephropathy only affects the kidneys, while IgA vasculitis can cause nephritic or nephrotic syndrome, and also presents with colicky abdominal pain, bloody stool, arthritis, and palpable skin lesions.

152
Q

What is the management for IgA neuropathy with low risk of progression?

A
  • No treatment needed
  • Follow up check for renal function.
153
Q

What is the management for IgA neuropathy with medium risk of progression?

A
  • ACEi / ABR for BP control.
154
Q

What is the management for IgA neuropathy with high risk of progression?

A
  • For patients with falling GRF or failing to respond to ACEi / ARB after 6 months
  • Corticosteroids

Other
- Statins
- Omega-3 fatty acids

155
Q

What are the complications of IgA neuropathy?

A
  • Hypertension
  • AKI
  • CKD
  • Nephrotic syndrome: uncommon and seen in < 10% of patients
  • Henoch-Schönlein purpura
156
Q

What is Goodpasture’s syndrome?

A
  • Goodpasture syndrome is an autoimmune disease that primarily affects the lungs and the kidneys.
  • Also known as anti-GBM disease and is a rare small-vessel vasculitis.
157
Q

What are the risk factors for Goodpasture’s syndrome?

A
  • HLA-DR15
  • Lymphocyte-depleting agents (e.g. alemtuzumab): loss of regulatory T cells
  • Infection
  • Smoking
  • Cocaine
  • Oxidative stress
  • Exposure to metal dust, organic solvents, or hydrocarbons
  • Alport syndrome: 5-10% of patients with Alport syndrome may develop anti-GBM disease following transplant.
158
Q

What are the constitutional symptoms of Goodpasture’s syndrome?

A
  • Lethargy
  • Fever
  • Anorexia
  • Weight loss
  • Myalgia
  • Arthralgia
159
Q

What are the kidney related clinical manifestations of Goodpasture’s syndrome?

A
  • Haematuria
  • Proteinuria
  • Oliguria/ anuria
  • Hypertension
160
Q

What are the lung related clinical manifestations of Goodpasture’s syndrome?

A
  • Cough
  • Shortness of breath
  • Haemoptysis
  • Pulmonary haemorrhage: may be seen on imaging

Usually present before kidney symptoms

161
Q

What are the investigations of Goodpasture’s syndrome?

A
  • Renal Biopsy - GOLD STANDARD
  • Anti-GBM antibody serologies

Acute renal screen
- Urinalysis
- Routine bloods
- Special bloods
- Imaging

162
Q

What are the differential diagnoses for Goodpasture’s syndrome?

A
  • Wegener’s granulomatosis
  • SLE
  • Microscopic polyangiitis
  • Churg-Strauss syndrome
163
Q

What is the management for Goodpasture’s syndrome?

A

FIRST LINE
- Corticosteroids
- Cyclophosphamide
- Plasmapheresis

Other
- Dialysis

164
Q

What are the complications of Goodpasture’s syndrome?

A
  • Chronic renal failure/ end-stage renal disease
  • Pulmonary haemorrhage
165
Q

What is SLE?

A

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune condition caused by a type 3 hypersensitivity reaction due to a complex interplay between genetic and environmental factors.

166
Q

What are the risk factors for SLE?

A
  • Middle-aged (14-45)
  • Female
  • African and Afro-Carribean
  • Family history
  • Drugs (procainamide, isoniazid, hydralazine)
  • HLA associations (HLA-B8, -DR2, -DR3)
167
Q

What are the clinical manifestations of SLE?

A

Presentation varies as SLE can affect many different organs. Mostly affects skin and joints.

168
Q

What are the investigations for SLE?

A

Bloods
- FBC
- U&Es
- ESR and CRP
- Clotting screen
- Complement C3 and C4

Antibodies
- ANA
- Anti-dsDNA
- Anti-Smith antibodies
- Anti-Ro and anti-La
- Anti-histone
- RF
- Anti-U1 RNP
- Antiphospholipid

  • Urinalysis
  • Skin or renal biopsy
  • Imaging
169
Q

What is the management of SLE?

A
  • Lifestyle changes
  • Mild cases: Prednisolone (corticosteroid) + hydroxychloroquine + NSAIDs
  • Moderate and severe: Prednisolone and hydroxychloroquine and an immunosuppressant

In severe cases, dialysis or kidney transplantation may be necessary.

170
Q

What is Diffuse proliferative glomerulonephritis (DPGN)?

A

Diffuse proliferative glomerulonephritis is the most common form of lupus nephritis.

171
Q

What are the risk factors for Diffuse proliferative glomerulonephritis (DPGN)?

A
  • Middle-aged (15-45)
  • Female gender
  • African and Afro-Caribbean
  • Family history
172
Q

What are the clinical manifestations of Diffuse proliferative glomerulonephritis (DPGN)?

A
  • Haematuria
  • Proteinuria
  • Hypertension
  • Oedema
  • Lethargy: linked to renal impairment
  • Signs of SLE: musculoskeletal pain; butterfly rash
173
Q

What are the investigations for Diffuse proliferative glomerulonephritis (DPGN)?

A
  • Renal biopsy - GOLD STANDARD
  • Urinalysis
  • U&Es
  • Renal USS
174
Q

What is the management for Diffuse proliferative glomerulonephritis (DPGN)?

A
  • Lifestyle changes
  • Pharmacology
    • Corticosteroids
    • Immunosuppressive agents
    • Hydroxychloroquine
  • Renal replacement therapy
  • ACEi
175
Q

What are the complications of Diffuse proliferative glomerulonephritis (DPGN)?

A

Renal failure

176
Q

What is RENAL DRS 26?

A
  • Mnemonic for assessment and management of acute kidney injury.
  • R - Record baseline creatinine (+ regular U&Es)
  • E - Exclude obstruction (clinical / USS)
  • N - Nephrotoxic drugs stopped
  • A - Assess fluid status
  • L - Losses +/- catheterisation
  • D - Dipstick (Blood +/- protein)
  • R - Review medications
  • S - Screen (consider acute renal screen)
  • 26 - Creatinine rise for AKI diagnosis
177
Q

What drugs should be stopped as they will worsen renal function in AKI?

A
  • NSAIDs (except aspirin at cardiac doses - 75mg)
  • Aminoglycosides
  • ACEi
  • Angiotensin II receptor antagonist
  • Diuretics
178
Q

What drugs may have to be stopped in AKI as they increase the risk of toxicity?

A
  • Metformin
  • Lithium
  • Digoxin
179
Q

What is the management for AKI?

A
  • Treat the underlying cause.
    • Fluid rehydration - IV fluids for pre-renal AKI
    • Stop nephrotoxic medication - e.g. NSAIDs and anti-hypertensives
    • Relieve obstruction in a post-renal AKI - e.g. catheter for patients with urinary retention from an enlarged prostate

Phase 2a Sheffield Medicine (10 decks)

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