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Renal Flashcards

1
Q

What are some causes of AKI? Categorise them

A

Prerenal:
- volume depletion
- reduced cardiac output
- systemic vasodilation => renal hypoperfusion
- drugs e.g. NSAIDs, ACE-i

Renal:
- acute tubular necrosis
- acute interstitial nephritis
- vascular
- glomerular

Postrenal:
- obstruction - stones, tumours, strictures, prostatic hypertrophy

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2
Q

What urine analysis findings can help investigate AKI?

A

🔹urine dipstick
- urinary tract infection: leucocytes +/- nitrites
- glomerulonephritis: haematuria + leucocytes
- acute interstitial nephritis: leucocytes by themselves

🔹microscopy, culture and sensitivity if any evidence of UTI on the urine dipstick

🔹protein:creatinine ratio if glomerulonephritis is suspected

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3
Q

What is the NICE criteria for diagnosis of AKI?

A

Any of the following:
🔹rise in serum Cr of >=26umol/L / 48hrs

🔹>50% inc in serum Cr over past 7 days

🔹UO < 0.5ml/kg/hr for >6 hrs

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4
Q

What is the RIFLE criteria? What is AKIN criteria?

A

RIFLE - Risk, Injury, Failure, Loss, End-stage renal disease
Uses serum Cr and UO to classify kidney injury
:::::
AKIN - uses stages 1-3 to classify AKI

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5
Q

What is the KDIGO classification?

A

Staging of AKI

1 = Cr x 1.5-1.9 or >26umol/L / 48 hrs
:: = UO < 0.5 ml/kg/hr > 6hrs

2 = Cr x 2.0-2.9
:: = UO < 0.5 ml/kg/hr >12hrs

3 = Cr x >3.0 baseline or >353.6 umol/L
:: = UO < 0.3 ml/kg/hr >24hr or anuria > 12hrs

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6
Q

What is the management of AKI?

A

Replace fluids
Hold nephrotoxics and review meds (NSAIDs, aminoglycosides, ACE-i, ARB, diuretics)
Treat underlying cause

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7
Q

What are some early and late clinical manifestations of CKD?

A

Early:
- fatigue (toxins, anaemia from reduced EPO)
- polyuria/nocturia
- HTN
- puffiness/swelling - fluid retention

Late:
- reduced UO
- fluid overload
- uraemia - N+V, anorexia, metallic taste, pruritis
- Neuro - poor concentration, fatigue, seizures, coma
- CVD
- anaemia
- bone and mineral disease - bone pain, fractures, renal osteodystrophy
- metabolic acidosis - Kussmaul breathing, confusion, lethargy

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8
Q

What causes anaemia in CKD?

A
  • reduced EPO levels
  • reduced erythropoiesis due to toxic effect of uraemia on bone marrow
  • reduced iron absorption
  • anorexia/nausea due to uraemia
  • reduced red cell survival
  • blood loss due to capillary fragility and poor platelet function
  • stress ulceration => blood loss
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9
Q

What is the management of mineral bone disease in CKD?

A

aim to reduce phosphate and PTH levels
- reduce dietary intake
- phosphate binders
- vitamin D
- parathyroidectomy in some cases

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10
Q

How do ACE inhibitors have a renoprotective effect, particularly in diabetic nephropathy?

A

They cause dilation of the efferent glomerular arterioles, reducing glomerular capillary pressure and protecting the filtration barriers.

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11
Q

What is the role of the glomerulus in the kidney?

A

It filters fluid from the capillaries into the renal tubule, the first step in urine formation.

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12
Q

What is nephritic syndrome? What are the key signs of nephritic syndrome?

A

A group of features associated with nephritis, including:
- haematuria
- oliguria
- proteinuria (<3g/day)
- fluid retention.

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13
Q

What is nephrotic syndrome? What are the key features of nephrotic syndrome?

A

A condition where the glomerular basement membrane becomes highly permeable, leading to significant proteinuria and associated features.

  • Massive Proteinuria (>3g/day)
  • Hypoalbuminaemia (<25g/L)
  • Peripheral oedema
  • Hypercholesterolaemia
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14
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease, which is usually idiopathic and responds well to steroids.

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15
Q

Name the top causes of nephrotic syndrome in adults.

A
  • Membranous nephropathy
  • Focal segmental glomerulosclerosis
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16
Q

What is IgA nephropathy, and who is typically affected?

A

Also known as Berger’s disease, it is the most common primary glomerulonephritis, usually affecting people in their 20s with haematuria.

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17
Q

What is membranous nephropathy, and what does histology show?

A

A cause of nephrotic syndrome in adults, involving immune deposits in the basement membrane. Histology shows IgG and complement deposits.

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18
Q

What is post-streptococcal glomerulonephritis?

A

A condition affecting people under 30, presenting 1-3 weeks after a streptococcal infection, with most patients making a full recovery.

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19
Q

What is Goodpasture syndrome, and what are its features?

A

Also known as anti-GBM disease, it involves anti-GBM antibodies attacking the glomerular and pulmonary basement membranes, causing acute kidney failure and haemoptysis.

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20
Q

Name systemic diseases that can cause glomerulonephritis.

A
  • Henoch-Schönlein purpura (HSP)
  • Vasculitis (e.g., microscopic polyangiitis, granulomatosis with polyangiitis)
  • Lupus nephritis
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21
Q

How can antibodies help differentiate conditions with acute kidney injury and haemoptysis?

A
  • Anti-GBM antibodies: Goodpasture syndrome
  • p-ANCA/MPO antibodies: Microscopic polyangiitis
  • c-ANCA/PR3 antibodies: Granulomatosis with polyangiitis
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22
Q

What are the main management approaches for glomerulonephritis?

A
  • Supportive care (e.g., blood pressure control, dialysis)
  • Immunosuppression (e.g., corticosteroids)
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23
Q

What is renal tubular acidosis (RTA)?

A

Metabolic acidosis due to pathology in the renal tubules, which disrupt the balance of hydrogen (H⁺) and bicarbonate (HCO₃⁻) ions between blood and urine.

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24
Q

What is the pathology, urinary pH and serum K in Type 1 renal tubular acidosis?

A

aka Distal RTA

Pathology: Distal tubule cannot excrete hydrogen ions

Urinary pH: High

Serum K: Low

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25
What is the pathology, urinary pH and serum K in Type 2 renal tubular acidosis?
aka proximal RTA Pathology: Proximal tubule cannot reabsorb bicarbonate Urinary pH: High Serum K: Low
26
What is the pathology, urinary pH and serum K in Type 4 renal tubular acidosis?
aka hyperkalaemic RTA Pathology: Low aldosterone or impaired aldosterone function Urinary pH: Low Serum K: High
27
What causes type 1 RTA?
- Genetic (autosomal dominant or recessive) - SLE - Sjögren’s syndrome - Primary biliary cholangitis - Hyperthyroidism - Sickle cell anaemia - Marfan’s syndrome
28
What is the biochemical presentation of Type 1 renal tubular acidosis?
- **High urinary pH** (above 6) due to the absence of hydrogen ions - **Metabolic acidosis**, due to retained hydrogen ions in the blood - **Hypokalaemia**, due to failure of the hydrogen and potassium exchange (H+/K+ ATPase)
29
What are the clinical features of type 1 RTA?
- Failure to thrive in children - Recurrent UTIs (due to alkaline urine) - Bone disease (rickets or osteomalacia) - Muscle weakness - Arrhythmias (due to hypokalaemia)
30
How is type 1 RTA treated?
Oral bicarbonate to correct acidosis and electrolyte imbalances.
31
What causes type 2 RTA?
- Genetic (autosomal dominant or recessive) - Multiple myeloma - Fanconi’s syndrome
32
What is the biochemical presentation of Type 2 renal tubular acidosis?
- High urinary pH (above 6) due to the excess bicarbonate in the urine - Metabolic acidosis, due to inadequate bicarbonate in the blood - Hypokalaemia, due to urinary loss of potassium along with bicarbonate
33
How is type 2 RTA treated?
Oral bicarbonate.
34
What is type 3 RTA?
A rare combination of type 1 and 2 RTA involving pathology in both the proximal and distal tubules.
35
What causes type 4 RTA?
- Adrenal insufficiency - Diabetic nephropathy - Medications (e.g., ACE inhibitors, spironolactone, or eplerenone)
36
What are the clinical features of type 4 RTA?
- Metabolic acidosis (retained hydrogen ions in blood) - Hyperkalaemia (retained potassium in blood) - Low urinary pH (reduced ammonia production in response to hyperkalaemia)
37
How is type 4 RTA managed?
- Treat the underlying cause - Fludrocortisone for aldosterone deficiency - Oral bicarbonate - Treatment of hyperkalaemia
38
What is haemolytic uraemic syndrome (HUS)?
A condition involving thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from E. coli O157 or Shigella.
39
Which patient population is most affected by HUS?
Children, typically following an episode of gastroenteritis.
40
What increases the risk of HUS in gastroenteritis caused by E. coli O157 or Shigella?
- Antibiotics - Anti-motility medications (e.g., loperamide)
41
What is the classic triad of features in HUS?
1. Microangiopathic haemolytic anaemia (MAHA) 2. Acute kidney injury (AKI) 3. Thrombocytopenia (low platelets)
42
How does HUS cause thrombocytopenia?
The formation of blood clots consumes platelets, reducing their availability in the bloodstream.
43
What causes acute kidney injury in HUS?
Thrombi and damaged red blood cells obstruct blood flow through the kidneys.
44
What is microangiopathic haemolytic anaemia (MAHA)?
Destruction of red blood cells due to pathology in small vessels where thrombi damage the red blood cells, causing haemolysis.
45
What is the typical progression of symptoms in HUS following gastroenteritis?
1. Diarrhoea (initial symptom, becomes bloody within 3 days) 2. Around 1 week later, features of HUS develop, including: - Fever - Abdominal pain - Lethargy - Pallor - Reduced urine output (oliguria) - Haematuria - Hypertension - Bruising - Jaundice (due to haemolysis) - Confusion
46
How is the causative organism in HUS identified?
Stool culture.
47
What is the management approach for HUS?
Hospital admission (HUS is a medical emergency) Supportive care for: - Hypovolaemia (IV fluids) - Hypertension - Severe anaemia (blood transfusions) - Severe renal failure (haemodialysis) Self-limiting disease
48
What are the key substances released from muscle cells during rhabdomyolysis?
- Myoglobin - Potassium (most immediately dangerous) - Phosphate - Creatine kinase
49
What is the primary renal complication of rhabdomyolysis?
AKI esp bc myoglobin
50
What are potential complications of rhabdomyolysis?
- Cardiac arrhythmia bc hyperkalaemia - AKI bc myoglobin - compartment syndrome - DIC
51
List some common causes of rhabdomyolysis.
- Prolonged immobility (e.g., frail patients after a fall) - Extremely rigorous exercise beyond fitness level (e.g., endurance events, CrossFit) - Crush injuries - Seizures - Statins
52
What are the main symptoms of rhabdomyolysis?
- Muscle pain, weakness, and swelling - Reduced urine output (oliguria) - Red-brown urine (myoglobinuria) - Fatigue - Nausea and vomiting - Confusion (particularly in frail patients)
53
What blood test is crucial for diagnosing rhabdomyolysis?
*Creatine kinase (CK)*: Normally <150 U/L; in rhabdomyolysis, it can range from *1,000-100,000 U/L.*
54
What is myoglobinuria, and how is it detected?
The presence of myoglobin in urine, giving it a red-brown color. It is detected with a urine dipstick that tests positive for blood.
55
Which investigations are necessary in rhabdomyolysis?
1. Creatine kinase (CK) to confirm the diagnosis. 2. Urea and electrolytes (U&E) to assess for acute kidney injury and hyperkalaemia. 3. ECG to monitor the effects of hyperkalaemia on the heart.
56
What is the primary treatment for rhabdomyolysis?
Intravenous fluids to correct hypovolaemia and promote filtration of breakdown products.
57
What additional treatments for rhabdomyolysis are debated and why?
- Intravenous sodium bicarbonate: To increase urinary pH and reduce the toxicity of myoglobin. - Intravenous mannitol: To increase urine output and reduce oedema. Both have associated risks and are not always recommended.
58
How is hyperkalaemia classified by serum potassium levels?
- Mild: 5.4 - 6 - Moderate: 6 - 6.5 - Severe - >6.5
59
List common causes of hyperkalaemia.
- Acute kidney injury - Chronic kidney disease (stage 4 or 5) - Rhabdomyolysis - Adrenal insufficiency - Tumour lysis syndrome
60
Which medications can cause hyperkalaemia? (4)
- Aldosterone antagonists (e.g., spironolactone, eplerenone) - ACE inhibitors (e.g., ramipril) - Angiotensin II receptor blockers (e.g., candesartan) - NSAIDs (e.g., naproxen)
61
What are the key ECG changes seen in hyperkalaemia?
- Tall peaked T waves - Flattening or absence of P waves - Prolonged PR interval - Broad QRS complexes
62
When does hyperkalaemia require urgent treatment?
- Serum potassium >6.5 mmol/L - Presence of ECG changes
63
What are the primary treatments for urgent hyperkalaemia?
- Insulin and dextrose infusion: Drives potassium into cells. - IV calcium gluconate: Stabilises cardiac muscle and prevents arrhythmias.
64
What additional treatments are available for hyperkalaemia?
- Nebulised salbutamol: Temporarily shifts potassium into cells. - Oral calcium resonium: Reduces GI potassium absorption (slow action, causes constipation). - Sodium bicarbonate: Used in acidosis (renal advice needed). - Haemodialysis: For severe or persistent hyperkalaemia.
65
What should be done for mild hyperkalaemia without ECG changes?
Address the underlying cause, such as: - Treating acute kidney injury. - Stopping causative medications (e.g., spironolactone, ACE inhibitors).
66
What is polycystic kidney disease (PKD)?
A genetic disorder where healthy kidney tissue is replaced with fluid-filled cysts, leading to renal failure. Enlarged kidneys may be palpable on abdominal examination.
67
Which genes are affected in Autosomal Dominant Polycystic Kidney Disease (ADPKD)?
- PKD1 on chromosome 16 (85% of cases) - PKD2 on chromosome 4 (15% of cases)
68
What are the extra-renal manifestations of AutDomPKD?
- Cerebral aneurysms - Hepatic, splenic, pancreatic, ovarian, and prostatic cysts - Mitral regurgitation - Colonic diverticula
69
What are the complications of ADPKD?
- Chronic loin/flank pain - Hypertension - Gross haematuria (from cyst rupture) - Recurrent urinary tract infections - Renal stones - End-stage renal failure (mean age ~50 years)
70
Which gene is affected in Autosomal Recessive Polycystic Kidney Disease (ARPKD)?
PKHD1 on chromosome 6.
71
How does ARPKD typically present?
Antenatal signs: Oligohydramnios (reduced amniotic fluid). Neonatal features: - Pulmonary hypoplasia (underdeveloped lungs) leading to respiratory failure. - Dysmorphic features: underdeveloped ear cartilage, low-set ears, flat nasal bridge. - End-stage renal failure often before adulthood.
72
How is PKD diagnosed?
- Ultrasound: Identifies kidney cysts. - Genetic testing: Confirms mutations in PKD1, PKD2, or PKHD1.
73
What is the role of tolvaptan in ADPKD?
A vasopressin receptor antagonist that slows the progression of cyst development and renal failure. Requires specific criteria and specialist monitoring.
74
What are the management strategies for PKD?
- Hypertension: ACE inhibitors (e.g., ramipril). - Pain management: Analgesia. - Infections: Antibiotics for UTIs or cyst infections. - Symptomatic cysts: Aspiration or surgical drainage. - Renal failure: Dialysis and/or renal transplant.
75
What are additional precautions in PKD management?
- Genetic counselling. - Avoiding contact sports (risk of cyst rupture). - Avoiding NSAIDs and anticoagulants. - MR angiography (MRA): Screen for cerebral aneurysms.

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