Renal Flashcards

1
Q

Q: What are the causes of normal anion gap (hyperchloraemic) metabolic acidosis?

A

Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison’s disease

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2
Q

Q: What conditions are associated with a raised anion gap in metabolic acidosis?

A

Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

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3
Q

Q: What causes metabolic alkalosis?

A

Metabolic alkalosis may be caused by a loss of hydrogen ions or a gain of bicarbonate, mainly due to problems in the kidney or gastrointestinal tract.

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4
Q

Q: What are the causes of metabolic alkalosis?

A

Vomiting/aspiration (e.g. peptic ulcer leading to pyloric stenosis, nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome
Congenital adrenal hyperplasia

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5
Q

Q: What are the common causes of respiratory acidosis?

A

COPD
Decompensation in other respiratory conditions (e.g. life-threatening asthma, pulmonary oedema)
Sedative drugs: benzodiazepines, opiate overdose

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6
Q

Q: What are the common causes of respiratory alkalosis?

A

Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
Altitude
Pregnancy

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7
Q

Q: What percentage of drug-induced acute kidney injury is accounted for by acute interstitial nephritis?

A

A: Acute interstitial nephritis accounts for 25% of drug-induced acute kidney injury.

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8
Q

Q: What are the common drug causes of acute interstitial nephritis?

A

Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide

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9
Q

Q: What systemic diseases can cause acute interstitial nephritis?

A

Systemic lupus erythematosus (SLE)
Sarcoidosis
Sjogren’s syndrome

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10
Q

Q: What infections can cause acute interstitial nephritis?

A

Hanta virus
Staphylococci

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11
Q

Q: What is seen in the histology of acute interstitial nephritis?

A

A: Marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules.

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12
Q

Q: What are the features of acute interstitial nephritis?

A

Fever
Rash
Arthralgia
Eosinophilia
Mild renal impairment
Hypertension

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13
Q

Q: What are the investigation findings in acute interstitial nephritis?

A

Sterile pyuria
White cell casts

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14
Q

Q: What are the symptoms of tubulointerstitial nephritis with uveitis (TINU)?

A

Fever
Weight loss
Painful, red eyes

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15
Q

Q: What is found on urinalysis in tubulointerstitial nephritis with uveitis (TINU)?

A

A: Urinalysis is positive for leukocytes and protein.

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16
Q

Q: What is one of the best ways to differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD)?

A

A: Renal ultrasound, as most patients with CKD have bilateral small kidneys.

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17
Q

Q: What are exceptions to the rule of bilateral small kidneys in CKD?

A

Autosomal dominant polycystic kidney disease
Diabetic nephropathy (early stages)
Amyloidosis
HIV-associated nephropathy

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18
Q

Q: What other feature suggests CKD rather than AKI?

A

A: Hypocalcaemia (due to lack of vitamin D).

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19
Q

Q: What does acute kidney injury (AKI) describe?

A

A: AKI describes a reduction in renal function following an insult to the kidneys.

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20
Q

Q: How are the causes of AKI traditionally divided?

A

A: Causes of AKI are divided into prerenal, intrinsic, and postrenal causes.

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21
Q

Q: What is a major cause of AKI?

A

A: Ischaemia (lack of blood flow) to the kidneys is a major cause of AKI.

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22
Q

Q: What are some examples of prerenal causes of AKI?

A

Hypovolaemia secondary to diarrhoea/vomiting
Renal artery stenosis

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23
Q

Q: What are some examples of intrinsic causes of AKI?

A

Glomerulonephritis
Acute tubular necrosis (ATN)
Acute interstitial nephritis (AIN)
Rhabdomyolysis
Tumour lysis syndrome

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24
Q

Q: What are some examples of postrenal causes of AKI?

A

Kidney stone in ureter or bladder
Benign prostatic hyperplasia
External compression of the ureter

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25
Q: Who is at an increased risk of AKI?
Chronic kidney disease Other organ failure/chronic disease (e.g., heart failure, liver disease, diabetes) History of AKI Use of nephrotoxic drugs (e.g., NSAIDs, aminoglycosides, ACE inhibitors) Use of iodinated contrast agents Age 65 years or over Oliguria Neurological/cognitive impairment or disability
26
Q: What are some preventive steps for AKI in at-risk patients?
Administering IV fluids for patients undergoing contrast investigations Temporarily stopping certain drugs like ACE inhibitors and ARBs
27
Q: What are the key functions of the kidneys that are affected in AKI?
Fluid balance Maintaining homeostasis (e.g., potassium, urea, creatinine balance)
28
Q: What are the key ways AKI may be detected?
Reduced urine output (oliguria) Fluid overload Rise in potassium, urea, or creatinine
29
Q: What are some symptoms and signs of AKI?
Reduced urine output Pulmonary and peripheral oedema Arrhythmias (secondary to potassium and acid-base balance changes) Features of uraemia (e.g., pericarditis, encephalopathy)
30
Q: What tests are commonly used to detect AKI?
Urea and electrolytes (U&Es) test: measures sodium, potassium, urea, and creatinine Urinalysis (for patients with suspected AKI) Renal ultrasound (if urinary tract obstruction is suspected)
31
Q: What are the criteria for diagnosing AKI according to NICE?
Rise in serum creatinine of 26 micromol/litre or greater within 48 hours 50% or greater rise in serum creatinine within the past 7 days Urine output less than 0.5 ml/kg/hour for more than 6 hours
32
Q: What is the management approach for AKI?
A: Management is largely supportive, involving careful fluid balance, medication review, and treatment of complications such as hyperkalaemia, pulmonary oedema, and acidosis.
33
Q: Which medications are usually safe to continue in AKI?
Paracetamol Warfarin Statins Aspirin (cardioprotective dose) Clopidogrel Beta-blockers
34
Q: Which medications should be stopped in AKI as they may worsen renal function?
NSAIDs (except for low-dose aspirin) Aminoglycosides ACE inhibitors Angiotensin II receptor antagonists Diuretics Metformin Lithium Digoxin
35
Q: How is hyperkalaemia treated in AKI?
Intravenous calcium gluconate Combined insulin/dextrose infusion Nebulised salbutamol Calcium resonium (orally or enema) Loop diuretics Dialysis
36
Q: When is renal replacement therapy (e.g., haemodialysis) used in AKI?
A: When the patient does not respond to medical treatment and is experiencing complications such as hyperkalaemia, pulmonary oedema, acidosis, or uraemia (e.g., pericarditis, encephalopathy).
37
Q: What is the urine sodium level in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: < 20 mmol/L Acute tubular necrosis: > 40 mmol/L
38
Q: What is the urine osmolality in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: > 500 mOsm/kg Acute tubular necrosis: < 350 mOsm/kg
39
Q: How does prerenal uraemia and acute tubular necrosis (ATN) respond to a fluid challenge?
Prerenal uraemia: Good response Acute tubular necrosis: Poor response
40
Q: What is the serum urea:creatinine ratio in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: Raised Acute tubular necrosis: Normal
41
Q: What is the fractional urea excretion in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: < 35% Acute tubular necrosis: > 35%
42
Q: What is the urine:plasma osmolality in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: > 1.5 Acute tubular necrosis: < 1.1
43
Q: What is the urine:plasma urea ratio in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: > 10:1 Acute tubular necrosis: < 8:1
44
Q: What is the specific gravity of urine in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: > 1020 Acute tubular necrosis: < 1010
45
Q: What does the urine look like in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: Normal or 'bland' sediment Acute tubular necrosis: Brown granular casts
46
Q: Why do the kidneys retain sodium in prerenal uraemia?
A: The kidneys hold on to sodium to preserve volume.
47
Q: What are the risk factors for AKI according to NICE guidelines?
Emergency surgery (risk of sepsis or hypovolaemia) Intraperitoneal surgery CKD (eGFR < 60) Diabetes Heart failure Age > 65 years Liver disease Use of nephrotoxic drugs: NSAIDs, aminoglycosides, ACE inhibitors/angiotensin II receptor antagonists, diuretics
48
Q: What are the diagnostic criteria for AKI according to NICE guidelines?
Rise in creatinine of 26µmol/L or more in 48 hours ≥ 50% rise in creatinine over 7 days Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) ≥ 25% fall in eGFR in children/young adults in 7 days
49
Q: What are the KDIGO staging criteria for Stage 1 AKI?
Increase in creatinine to 1.5-1.9 times baseline Increase in creatinine by ≥26.5 µmol/L Reduction in urine output to < 0.5 mL/kg/hour for ≥ 6 hours
50
Q: What are the KDIGO staging criteria for Stage 2 AKI?
Increase in creatinine to 2.0 to 2.9 times baseline Reduction in urine output to < 0.5 mL/kg/hour for ≥12 hours
51
Q: What are the KDIGO staging criteria for Stage 3 AKI?
Increase in creatinine to ≥ 3.0 times baseline, or Increase in creatinine to ≥353.6 µmol/L, or Reduction in urine output to < 0.3 mL/kg/hour for ≥24 hours, or The initiation of kidney replacement therapy, or In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m²
52
Q: When should a patient with AKI be referred to a nephrologist?
Renal transplant ITU patient with unknown cause of AKI Vasculitis/glomerulonephritis/tubulointerstitial nephritis/myeloma AKI with no known cause Inadequate response to treatment Complications of AKI Stage 3 AKI CKD stage 4 or 5 Complications like hyperkalaemia, metabolic acidosis, uraemia, or fluid overload (pulmonary oedema)
53
Q: What is the most common inherited cause of kidney disease?
A: Autosomal Dominant Polycystic Kidney Disease (ADPKD).
54
Q: Which gene loci are associated with ADPKD?
A: PKD1 and PKD2, which code for polycystin-1 and polycystin-2, respectively.
55
Q: What is the difference between ADPKD type 1 and ADPKD type 2?
ADPKD type 1: 85% of cases, located on chromosome 16, presents with renal failure earlier. ADPKD type 2: 15% of cases, located on chromosome 4.
56
Q: What is the screening investigation for relatives of ADPKD patients?
A: Abdominal ultrasound.
57
Q: What are the ultrasound diagnostic criteria for ADPKD in patients with a positive family history?
< 30 years: Two cysts, unilateral or bilateral. 30-59 years: Two cysts in both kidneys. 60 years: Four cysts in both kidneys.
58
Q: When is tolvaptan (vasopressin receptor 2 antagonist) recommended for treating ADPKD?
For patients with chronic kidney disease stage 2 or 3 at the start of treatment. If there is evidence of rapidly progressing disease. If the company provides it with the agreed discount in the patient access scheme.
59
Q: What are the findings in an ADPKD kidney on imaging?
A: Extensive cysts are seen in an enlarged kidney.
60
Q: What are the common renal features of ADPKD?
Hypertension Recurrent UTIs Flank pain Haematuria Palpable kidneys Renal impairment Renal stones
61
Q: What are the extra-renal manifestations of ADPKD?
Liver cysts (70%, may cause hepatomegaly) Berry aneurysms (8%, risk of subarachnoid haemorrhage) Cardiovascular: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection Cysts in other organs: pancreas, spleen (rarely thyroid, oesophagus, ovary)
62
Q: What is the inheritance pattern of Alport's syndrome?
A: Alport's syndrome is usually inherited in an X-linked dominant pattern.
63
Q: What is the underlying cause of Alport's syndrome?
A: Alport's syndrome is caused by a defect in the gene that codes for type IV collagen, leading to an abnormal glomerular-basement membrane (GBM).
64
Q: Why is Alport's syndrome more severe in males?
A: Males have only one X chromosome, so the defect is typically more severe in them, while females rarely develop renal failure due to having a second, unaffected X chromosome.
65
Q: What complications can occur in a renal transplant recipient with Alport's syndrome?
A: The presence of anti-GBM antibodies can lead to a Goodpasture's syndrome-like picture.
66
Q: What are the typical presenting features of Alport's syndrome in childhood?
Microscopic haematuria Progressive renal failure Bilateral sensorineural deafness Lenticonus (protrusion of the lens surface into the anterior chamber) Retinitis pigmentosa
67
Q: What is the characteristic finding on renal biopsy for Alport's syndrome?
A: Splitting of the lamina densa, visible on electron microscopy, resulting in a 'basket-weave' appearance.
68
Q: What diagnostic tests are used to confirm Alport's syndrome?
Molecular genetic testing Renal biopsy Electron microscopy (for basket-weave appearance)
69
Q: What does amyloidosis refer to?
A: Amyloidosis refers to the extracellular deposition of an insoluble fibrillar protein termed amyloid, which leads to tissue or organ dysfunction.
70
Q: How is amyloid typically classified?
A: Amyloidosis is classified as systemic or localized, and further characterized by the precursor protein (e.g., AL in myeloma, where A stands for amyloid and L stands for immunoglobulin light chain fragments).
71
Q: What is the diagnostic method for amyloidosis?
Congo red staining (apple-green birefringence) Serum amyloid precursor (SAP) scan Biopsy of skin, rectal mucosa, or abdominal fat
72
Q: How is the anion gap calculated?
(Sodium + Potassium) - (Bicarbonate + Chloride)
73
Q: What is the normal range for the anion gap?
A: The normal anion gap is 8-14 mmol/L.
74
Q: What causes a normal anion gap or hyperchloraemic metabolic acidosis?
Gastrointestinal bicarbonate loss (e.g., diarrhea, ureterosigmoidostomy, fistula) Renal tubular acidosis Drugs (e.g., acetazolamide, ammonium chloride injection) Addison's disease
75
Q: What causes a raised anion gap metabolic acidosis?
Lactate (e.g., shock, hypoxia) Ketones (e.g., diabetic ketoacidosis, alcohol) Urate (e.g., renal failure) Acid poisoning (e.g., salicylates, methanol) 5-oxoproline (e.g., chronic paracetamol use)
76
Q: What is Anti-glomerular Basement Membrane (GBM) disease (Goodpasture's syndrome)?
A: Anti-glomerular Basement Membrane (GBM) disease is a rare type of small-vessel vasculitis associated with both pulmonary hemorrhage and rapidly progressive glomerulonephritis. It is caused by anti-GBM antibodies against type IV collagen.
77
Q: What are the common features of Goodpasture's syndrome?
Pulmonary hemorrhage Rapidly progressive glomerulonephritis (acute kidney injury) Nephritis → Proteinuria + Hematuria
78
Q: What are the typical age groups for Goodpasture's syndrome?
A: Goodpasture's syndrome has a bimodal age distribution, with peaks in the 20-30 and 60-70 age brackets.
79
Q: What genetic association is linked to Goodpasture's syndrome?
A: It is associated with HLA DR2.
80
Q: What are the typical investigations for Goodpasture's syndrome?
Renal biopsy: Linear IgG deposits along the basement membrane Raised transfer factor secondary to pulmonary hemorrhages
81
Q: What is the main treatment for Goodpasture's syndrome?
Plasma exchange (plasmapheresis) Steroids Cyclophosphamide
82
Q: What are the factors that increase the likelihood of pulmonary hemorrhage in Goodpasture's syndrome?
Smoking Lower respiratory tract infection Pulmonary edema Inhalation of hydrocarbons Young males
83
Q: What is Autosomal Recessive Polycystic Kidney Disease (ARPKD)?
A: ARPKD is a much less common form of polycystic kidney disease than autosomal dominant polycystic kidney disease (ADPKD). It is due to a defect in a gene located on chromosome 6 that encodes fibrocystin, a protein important for normal renal tubule development.
84
Q: How is ARPKD diagnosed?
A: Diagnosis may be made on prenatal ultrasound or in early infancy with abdominal masses and renal failure. Newborns may also show features consistent with Potter's syndrome secondary to oligohydramnios.
85
Q: What are the typical renal findings in ARPKD?
A: Renal findings include abdominal masses and renal failure, with end-stage renal failure developing in childhood.
86
Q: What other organ is typically involved in ARPKD?
A: Liver involvement is typical, such as portal and interlobular fibrosis.
87
Q: What is the characteristic finding in renal biopsy in ARPKD?
A: Renal biopsy typically shows multiple cylindrical lesions at right angles to the cortical surface.
88
Q: What is an arteriovenous fistula?
A: An arteriovenous fistula is a direct connection between an artery and a vein. It can occur pathologically but is usually surgically created for haemodialysis access.
89
Q: How long does it take for an arteriovenous fistula to develop?
A: It typically takes 6 to 8 weeks for an arteriovenous fistula to mature and become ready for use.
90
Q: What are the potential complications of arteriovenous fistulas?
A: Potential complications include infection, thrombosis, stenosis, steal syndrome, and the absence of a bruit which may indicate issues with the fistula.
91
Q: What is steal syndrome in the context of arteriovenous fistulas?
A: Steal syndrome occurs when blood is diverted from the distal limb to the fistula, leading to symptoms such as acute limb pain.
92
Q: What is the most significant cause of anaemia in chronic kidney disease (CKD)?
A: The most significant cause of anaemia in CKD is reduced erythropoietin levels, which are responsible for stimulating red blood cell production in the bone marrow.
93
Q: When does anaemia typically become apparent in CKD patients?
A: Anaemia in CKD usually becomes apparent when the glomerular filtration rate (GFR) is less than 35 ml/min. Other causes of anaemia should be considered if the GFR is > 60 ml/min.
94
Q: How does anaemia in CKD affect the heart?
A: Anaemia in CKD predisposes to the development of left ventricular hypertrophy, which is associated with a three-fold increase in mortality in renal patients.
95
Q: What is the role of hepcidin in anaemia in CKD?
A: In CKD, hepcidin levels are elevated due to inflammation and reduced renal clearance. This leads to decreased iron absorption from the gut and impaired release of stored iron from macrophages and hepatocytes, reducing iron available for erythropoiesis.
96
Q: What is the effect of metabolic acidosis in CKD on iron absorption?
A: Metabolic acidosis in CKD can inhibit the conversion of ferric iron (Fe³⁺) to its absorbable form, ferrous iron (Fe²⁺), in the duodenum, leading to reduced iron absorption.
97
Q: What should be done before administering erythropoiesis-stimulating agents (ESA) for anaemia in CKD?
A: Iron status should be determined and optimised before the administration of erythropoiesis-stimulating agents (ESA).
98
Q: What is the recommended haemoglobin target for patients with CKD anaemia according to NICE guidelines?
A: The 2011 NICE guidelines suggest a target haemoglobin of 10 - 12 g/dL.
99
Q: How should anaemia in CKD be managed?
Oral iron for patients not on ESAs or haemodialysis. IV iron if target haemoglobin levels are not reached with oral iron within 3 months or for patients on ESAs or haemodialysis. ESAs like erythropoietin and darbepoetin should be used for patients who are likely to benefit in terms of quality of life and physical function.
100
Q: What are the basic problems that contribute to bone disease in chronic kidney disease (CKD)?
Low vitamin D (due to impaired 1-alpha hydroxylation in the kidneys). High phosphate. Low calcium (due to lack of vitamin D and high phosphate). Secondary hyperparathyroidism (due to low calcium, high phosphate, and low vitamin D).
101
Q: What is osteitis fibrosa cystica, and what causes it in CKD?
A: Osteitis fibrosa cystica, also known as hyperparathyroid bone disease, is a condition associated with secondary hyperparathyroidism in CKD. It results from high phosphate and low calcium, which lead to overactivity of parathyroid glands and bone resorption.
102
Q: What is adynamic bone disease in CKD?
A: Adynamic bone disease is characterized by a reduction in cellular activity (both osteoblasts and osteoclasts) in bone. It may be due to over-treatment with vitamin D, leading to suppressed parathyroid hormone (PTH) secretion and diminished bone turnover.
103
Q: What is osteomalacia, and how does it develop in CKD?
A: Osteomalacia is the softening of bones due to inadequate mineralization, commonly caused by low vitamin D levels in CKD. It leads to defective bone mineralization and bone pain.
104
Q: How does osteosclerosis manifest in CKD?
A: Osteosclerosis in CKD is characterized by increased bone density, often as a response to hyperparathyroidism, but it can also be associated with disordered bone mineralization and structural changes in bones.
105
Q: What is osteoporosis in the context of CKD?
A: Osteoporosis in CKD refers to reduced bone mass and increased fracture risk, which can occur due to low calcium, vitamin D deficiency, and secondary hyperparathyroidism.
106
Q: What is a "brown tumour" in the context of CKD bone disease?
A: A brown tumour is a radiographic finding seen in secondary hyperparathyroidism due to CKD. It results from cystic bone lesions formed by excessive parathyroid hormone secretion, often seen in the long bones and jaws.
107
Q: What is the most common cause of chronic kidney disease (CKD)?
A: The most common cause of CKD is diabetic nephropathy, which occurs due to damage to the kidneys' blood vessels caused by prolonged high blood sugar in diabetes.
108
Q: How does chronic glomerulonephritis contribute to CKD?
A: Chronic glomerulonephritis is a long-term inflammation of the glomeruli (kidney filtering units), which leads to progressive kidney damage and scarring, ultimately causing CKD.
109
Q: How does chronic pyelonephritis lead to CKD?
A: Chronic pyelonephritis is a long-standing kidney infection that causes scarring of the renal parenchyma and can eventually lead to CKD due to repeated infections and inflammation.
110
Q: How does hypertension contribute to CKD?
A: Hypertension (high blood pressure) can damage the kidneys' blood vessels, leading to glomerulosclerosis and decreased kidney function, which over time can cause CKD.
111
Q: How does adult polycystic kidney disease (APKD) contribute to CKD?
A: APKD is a genetic disorder where multiple cysts form in the kidneys, progressively enlarging the kidneys and causing kidney dysfunction, leading to CKD as the cysts grow and compress kidney tissue.
112
Q: Why is serum creatinine not always an accurate estimate of renal function?
A: Serum creatinine may not provide an accurate estimate of renal function due to differences in muscle mass, which affects creatinine levels. Therefore, formulas like the MDRD equation are used to estimate the glomerular filtration rate (eGFR).
113
Q: What variables are used in the Modification of Diet in Renal Disease (MDRD) equation to estimate eGFR?
A: The MDRD equation uses serum creatinine, age, gender, and ethnicity to estimate eGFR.
114
Q: What factors can affect eGFR calculation?
A: Factors affecting eGFR include pregnancy, muscle mass (e.g., in amputees or bodybuilders), and eating red meat 12 hours before the sample is taken.
115
Q: How is chronic kidney disease (CKD) classified based on eGFR?
Stage 1: eGFR > 90 ml/min with kidney damage Stage 2: eGFR 60-89 ml/min with kidney damage Stage 3a: eGFR 45-59 ml/min (moderate reduction) Stage 3b: eGFR 30-44 ml/min (moderate reduction) Stage 4: eGFR 15-29 ml/min (severe reduction) Stage 5: eGFR < 15 ml/min (kidney failure, dialysis or transplant needed)
116
Q: How is chronic kidney disease (CKD) usually diagnosed?
A: CKD is usually asymptomatic and is diagnosed following abnormal urea and electrolyte results.
117
Q: What are some possible symptoms of late-stage chronic kidney disease (CKD)?
Oedema (e.g., ankle swelling, weight gain) Polyuria Lethargy Pruritus (secondary to uraemia) Anorexia, leading to weight loss Insomnia Nausea and vomiting Hypertension
118
Q: What is the first-line treatment for hypertension in chronic kidney disease (CKD)?
A: ACE inhibitors are first-line treatment, especially in proteinuric renal disease (e.g., diabetic nephropathy).
119
Q: What is the expected effect on glomerular filtration rate (GFR) when using ACE inhibitors in CKD patients?
A: ACE inhibitors can reduce filtration pressure, leading to a small fall in GFR and a rise in creatinine. A decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, but any rise should prompt careful monitoring and exclusion of other causes.
120
Q: What medication is useful for treating hypertension in CKD when the GFR falls below 45 ml/min?
A: Furosemide is useful, particularly when GFR is below 45 ml/min. It helps lower serum potassium but requires high doses and careful monitoring for dehydration.
121
Q: What are the basic pathophysiological problems in CKD that affect mineral bone health?
Low vitamin D due to reduced 1-alpha hydroxylation in the kidneys. High phosphate levels due to reduced phosphate excretion by the kidneys.
122
Q: What complications arise from high phosphate and low calcium in CKD?
Osteomalacia (due to phosphate 'dragging' calcium from bones) Secondary hyperparathyroidism (due to low calcium, high phosphate, and low vitamin D)
123
Q: What is the primary aim of managing mineral bone disease in CKD?
A: The primary aim is to reduce phosphate and parathyroid hormone (PTH) levels.
124
Q: What is the first-line management for mineral bone disease in CKD?
Reduced dietary phosphate intake Phosphate binders Vitamin D (alfacalcidol, calcitriol)
125
Q: When might parathyroidectomy be considered in CKD patients with mineral bone disease?
A: Parathyroidectomy may be required in cases where medical management is not effective in controlling secondary hyperparathyroidism.
126
Q: Why is proteinuria an important marker in CKD, especially in diabetic nephropathy?
A: Proteinuria indicates kidney damage and is used to assess the progression of CKD. It is especially important in diabetic nephropathy, where it reflects glomerular damage and worsening renal function.
127
Q: Which ratio is preferred by NICE for identifying proteinuria, and why?
A: The albumin:creatinine ratio (ACR) is preferred over the protein:creatinine ratio (PCR) because it has greater sensitivity for detecting proteinuria, particularly in diabetics.
128
Q: How should an ACR sample be collected for accurate results?
Collect a spot sample to avoid 24-hour urine collection. The sample should be first-pass morning urine. If the initial ACR is between 3 and 70 mg/mmol, confirm with a subsequent early morning sample. No repeat sample is needed if ACR is ≥ 70 mg/mmol.
129
Q: What is the clinically significant threshold for ACR according to NICE?
A: A confirmed ACR of 3 mg/mmol or more is regarded as clinically significant proteinuria.
130
Q: When should a nephrologist be referred for proteinuria, according to NICE guidelines?
ACR ≥ 70 mg/mmol (unless caused by diabetes and already treated) ACR ≥ 30 mg/mmol with persistent haematuria (after excluding urinary tract infection) ACR 3-29 mg/mmol with persistent haematuria and other risk factors (e.g., declining eGFR or cardiovascular disease)
131
Q: What is the frequency of eGFR and ACR monitoring for patients at risk of CKD?
G1 (eGFR ≥ 90): Monitor ACR < 1 G2 (eGFR 60-89): Monitor ACR < 1 G3a (eGFR 45-59): Monitor ACR 1 G3b (eGFR 30-44): Monitor ACR < 2 G4 (eGFR 15-29): Monitor ACR 2 G5 (eGFR < 15): Monitor ACR ≥ 4
132
Q: What are the first-line treatments for proteinuria in CKD?
ACE inhibitors or angiotensin II receptor blockers (ARB) should be used in patients with CKD and hypertension if ACR > 30 mg/mmol. If ACR > 70 mg/mmol, these medications are indicated regardless of blood pressure.
133
Q: How do SGLT2 inhibitors help in the management of proteinuria in CKD?
SGLT2 inhibitors block glucose reabsorption in the proximal tubule, leading to glycosuria and lowering the renal glucose threshold. They reduce sodium reabsorption, promoting natriuresis, lowering blood pressure, and reducing intraglomerular pressure via normalized tubuloglomerular feedback.
134
Q: What is the main difference between cranial and nephrogenic diabetes insipidus (DI)?
Cranial DI is caused by decreased secretion of antidiuretic hormone (ADH) from the pituitary. Nephrogenic DI is caused by insensitivity to ADH in the kidneys.
135
Q: What are some common causes of cranial diabetes insipidus (DI)?
Idiopathic Post head injury Pituitary surgery Craniopharyngiomas Infiltrative diseases: Histiocytosis X, sarcoidosis, hemachromatosis DIDMOAD (Wolfram's syndrome): diabetes mellitus, optic atrophy, deafness
136
Q: What are some common causes of nephrogenic diabetes insipidus (DI)?
Genetic: mutation in vasopressin receptor or aquaporin 2 channel Electrolyte disturbances: hypercalcemia, hypokalemia Medications: Lithium, demeclocycline Tubulo-interstitial diseases: obstruction, sickle-cell disease, pyelonephritis
137
Q: What are the main clinical features of diabetes insipidus?
Polyuria (excessive urination) Polydipsia (excessive thirst)
138
Q: What are the typical investigation findings in diabetes insipidus?
High plasma osmolality Low urine osmolality Urine osmolality >700 mOsm/kg excludes DI Water deprivation test may be used to differentiate types.
139
Q: What is the management for nephrogenic diabetes insipidus?
Thiazide diuretics Low salt/protein diet
140
Q: How is central diabetes insipidus treated?
Desmopressin (synthetic ADH)
141
Q: How should patients with diabetic nephropathy be screened annually?
Use urinary albumin:creatinine ratio (ACR) The sample should be an early morning specimen An ACR > 2.5 indicates microalbuminuria.
142
Q: What are the key components of managing diabetic nephropathy?
Dietary protein restriction Tight glycaemic control Blood pressure control: aim for < 130/80 mmHg ACE inhibitor or angiotensin-II receptor antagonist: start if ACR ≥ 3 mg/mmol Statins to control dyslipidaemia
143
Q: What is the target blood pressure for managing diabetic nephropathy?
< 130/80 mmHg
144
Q: When should ACE inhibitors or angiotensin-II receptor antagonists be started in diabetic nephropathy management?
When urinary ACR is ≥ 3 mg/mmol.
145
Q: Why should dual therapy with ACE inhibitors and angiotensin-II receptor antagonists not be started in diabetic nephropathy?
Dual therapy increases the risk of hyperkalemia and acute kidney injury.
146
Q: What is the primary function of erythropoietin?
Erythropoietin is a haematopoietic growth factor that stimulates the production of erythrocytes (red blood cells) in response to cellular hypoxia.
147
Q: What are the common side-effects of erythropoietin?
Accelerated hypertension (leading to encephalopathy and seizures 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., in dialysis fistula) Iron deficiency secondary to increased erythropoiesis
148
Q: What are some reasons why patients may fail to respond to erythropoietin therapy?
Iron deficiency Inadequate dose Concurrent infection/inflammation Hyperparathyroid bone disease Aluminium toxicity
149
Q: How does darbepoetin differ from erythropoietin?
Darbepoetin carries a reduced risk of pure red cell aplasia compared to erythropoietin.
150
Q: What is Fanconi syndrome?
Fanconi syndrome is a generalized reabsorptive disorder of renal tubular transport in the proximal convoluted tubule, leading to several abnormalities in the kidney's ability to reabsorb substances.
151
Q: What are the main features of Fanconi syndrome?
Type 2 (proximal) renal tubular acidosis Polyuria Aminoaciduria Glycosuria Phosphaturia Osteomalacia (due to phosphate loss)
152
Q: What are some common causes of Fanconi syndrome?
Cystinosis (most common cause in children) Sjogren's syndrome Multiple myeloma Nephrotic syndrome Wilson's disease
153
Q: What is fibromuscular dysplasia?
Fibromuscular dysplasia is a condition that causes abnormal growth or development of the artery walls, leading to renal artery stenosis. It accounts for 10% of renal vascular disease, with atherosclerosis causing the remaining 90%.
154
Q: What are the features of fibromuscular dysplasia?
Hypertension Chronic kidney disease or acute renal failure (e.g., secondary to ACE-inhibitor initiation) "Flash" pulmonary oedema (sudden onset)
155
Q: What is the recommended amount of maintenance fluids for adults according to the 2013 NICE guidelines?
25-30 ml/kg/day of water Approximately 1 mmol/kg/day of potassium, sodium, and chloride Approximately 50-100 g/day of glucose to limit starvation ketosis
156
Q: What is the fluid regimen recommended by NICE for the first 24 hours for routine maintenance fluids?
Sodium chloride 0.18% in 4% glucose with 27 mmol/L potassium
157
Q: What is a potential complication of using 0.9% saline for large volumes of fluid replacement?
Increased risk of hyperchloraemic metabolic acidosis.
158
Q: What is Focal Segmental Glomerulosclerosis (FSGS) and what does it cause?
FSGS is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.
159
Q: What are the causes of Focal Segmental Glomerulosclerosis (FSGS)?
Idiopathic Secondary causes: IgA nephropathy Reflux nephropathy HIV Heroin use Alport's syndrome Sickle-cell disease
160
Q: Why is Focal Segmental Glomerulosclerosis noted to have a high recurrence rate?
FSGS has a high recurrence rate in renal transplants.
161
Q: What are the investigations for diagnosing Focal Segmental Glomerulosclerosis?
Renal biopsy Light microscopy: focal and segmental sclerosis and hyalinosis Electron microscopy: effacement of foot processes
162
Q: What is the management for Focal Segmental Glomerulosclerosis (FSGS)?
Steroids ± immunosuppressants.
163
Q: What are the causes of transient or spurious non-visible haematuria?
Urinary tract infection (UTI) Menstruation Vigorous exercise (settles in ~3 days) Sexual intercourse
164
Q: What are the causes of persistent non-visible haematuria?
Cancer: Bladder, renal, prostate Stones Benign prostatic hyperplasia Prostatitis Urethritis (e.g., Chlamydia) Renal causes: IgA nephropathy Thin basement membrane disease
165
Q: What are the spurious causes of red/orange urine that are not due to blood?
Foods: Beetroot, rhubarb Drugs: Rifampicin, doxorubicin
166
Q: What are the key points in the management of haematuria?
No evidence to support screening for haematuria. Incidence is similar in patients on aspirin/warfarin to the general population, and they should also be investigated. Testing: Urine dipstick is the test of choice. Persistent non-visible haematuria is blood present in 2 out of 3 samples tested 2-3 weeks apart. Check renal function, ACR, PCR, and blood pressure. Urine microscopy may be used but time affects red blood cell detection.
167
Q: What are the NICE urgent cancer referral guidelines for haematuria?
Urgent referral (within 2 weeks): Aged >= 45 years AND: Unexplained visible haematuria without UTI, or Visible haematuria that persists or recurs after successful UTI treatment. Aged >= 60 years AND unexplained non-visible haematuria with dysuria or a raised white cell count.
168
Q: What is the non-urgent referral guideline for haematuria in patients aged 60 or older?
Aged 60 or older with recurrent or persistent unexplained UTI.
169
Q: What is the general approach for managing non-visible haematuria in patients under 40 years old?
No referral needed if: Normal renal function No proteinuria Normotensive These patients may be managed in primary care.
170
Q: What is the classic triad of Haemolytic Uraemic Syndrome (HUS)?
Acute kidney injury Microangiopathic haemolytic anaemia (MAHA) Thrombocytopenia
171
Q: What is the most common cause of secondary (typical) HUS, particularly in children?
Shiga toxin-producing Escherichia coli (STEC) 0157:H7, also known as verotoxigenic or enterohaemorrhagic E. coli. Accounts for over 90% of cases in children.
172
Q: What are some other causes of secondary HUS besides STEC infection?
Pneumococcal infection HIV Rare causes: Systemic lupus erythematosus (SLE) Drugs Cancer
173
Q: What is primary (atypical) HUS caused by?
Complement dysregulation.
174
Q: What is the most useful initial diagnostic test for Haemolytic Uraemic Syndrome (HUS)?
Blood film: Shows MAHA (Coombs-negative haemolysis) Intravascular red blood cell fragmentation → formation of schistocytes.
175
Q: What are the typical lab findings in HUS?
Anaemia: Hb < 8 g/dL Thrombocytopenia U&E: Shows acute kidney injury Stool culture: For evidence of STEC infection PCR for Shiga toxins
176
Q: What is the management of Haemolytic Uraemic Syndrome (HUS)?
Supportive treatment: Fluids Blood transfusions Dialysis if required No role for antibiotics despite preceding diarrhoeal illness in many cases.
177
Q: What is the cause of Henoch-Schonlein Purpura (HSP)?
IgA-mediated small vessel vasculitis. There is some overlap with IgA nephropathy (Berger's disease).
178
Q: What are the features of Henoch-Schonlein Purpura (HSP)?
Palpable purpuric rash with localized oedema over: Buttocks Extensor surfaces of arms and legs Abdominal pain Polyarthritis Features of IgA nephropathy may occur, such as: Haematuria Renal failure
179
Q: What is the treatment for Henoch-Schonlein Purpura (HSP)?
Analgesia for arthralgia Nephropathy treatment: Generally supportive Inconsistent evidence for the use of: Steroids Immunosuppressants
180
Q: What is the cause of renal involvement in HIV patients?
Renal involvement may occur as a consequence of: HIV itself Antiretroviral treatment (e.g., protease inhibitors such as indinavir can precipitate intratubular crystal obstruction).
181
Q: What is HIV-associated nephropathy (HIVAN)?
HIVAN accounts for up to 10% of end-stage renal failure cases in the United States. Antiretroviral therapy is the treatment of choice. Adherence to antiretroviral therapy should be checked if the patient is already on it.
182
Q: What are the five key features of HIV-associated nephropathy (HIVAN)?
Massive proteinuria, resulting in nephrotic syndrome Normal or large kidneys Focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy Elevated urea and creatinine Normotension
183
Q: What is the classification of hyperkalaemia?
Mild: 5.5 - 5.9 mmol/L Moderate: 6.0 - 6.4 mmol/L Severe: ≥ 6.5 mmol/L ECG changes are important in determining management and should be done in all new cases of hyperkalaemia.
184
Q: What ECG changes are associated with hyperkalaemia?
Peaked or 'tall-tented' T waves (occurs first) Loss of P waves Broad QRS complexes Sinusoidal wave pattern
185
Q: What are the principles of treatment for hyperkalaemia?
Stabilisation of the cardiac membrane: IV calcium gluconate (does not lower potassium levels) Short-term shift of potassium from extracellular to intracellular compartment: Insulin/dextrose infusion Nebulised salbutamol Removal of potassium from the body: Calcium resonium (oral/enema) Loop diuretics Dialysis Haemofiltration/haemodialysis for AKI with persistent hyperkalaemia
186
Q: What is the initial management for severe hyperkalaemia (≥6.5 mmol/L) or hyperkalaemia with ECG changes?
IV calcium gluconate: To stabilise the myocardium Insulin/dextrose infusion: Short-term potassium shift Nebulised salbutamol: To temporarily lower serum potassium
187
Q: What are the further management steps for hyperkalaemia?
Stop exacerbating drugs (e.g., ACE inhibitors) Treat underlying cause Lower total body potassium using: Calcium resonium Loop diuretics Dialysis
188
Q: What are the features of hypokalaemia?
Muscle weakness Hypotonia Predisposition to digoxin toxicity (especially in patients on diuretics)
189
Q: What ECG features are associated with hypokalaemia?
U waves Small or absent T waves Prolonged PR interval ST depression
190
Q: What is IgA nephropathy also known as?
A: Berger's disease.
191
Q: What is the commonest cause of glomerulonephritis worldwide?
A: IgA nephropathy (Berger's disease).
192
Q: What are some associated conditions with IgA nephropathy?
Alcoholic cirrhosis Coeliac disease/dermatitis herpetiformis Henoch-Schonlein purpura
193
Q: What is the pathophysiology of IgA nephropathy?
Caused by mesangial deposition of IgA immune complexes There is pathological overlap with Henoch-Schonlein purpura (HSP).
194
Q: What are the histological features of IgA nephropathy?
Mesangial hypercellularity Positive immunofluorescence for IgA and C3
195
Q: How does IgA nephropathy typically present?
Young male Recurrent macroscopic haematuria Typically associated with a recent respiratory tract infection Nephrotic range proteinuria is rare Renal failure is unusual and seen in a minority of patients
196
Q: How can IgA nephropathy be differentiated from post-streptococcal glomerulonephritis?
Post-streptococcal glomerulonephritis has low complement levels In post-streptococcal glomerulonephritis, proteinuria is the main symptom (though haematuria can occur) In IgA nephropathy, haematuria is more prominent, typically following a URTI, and the onset of renal problems occurs soon after.
197
Q: What is the initial treatment for persistent proteinuria in IgA nephropathy?
ACE inhibitors.
198
Q: What should be done if there is active disease or failure to respond to ACE inhibitors in IgA nephropathy?
Immunosuppression with corticosteroids.
199
Q: How does Membranoproliferative Glomerulonephritis typically present?
Nephrotic syndrome Haematuria Proteinuria
200
Q: What are the types of Membranoproliferative Glomerulonephritis?
Type 1 Type 2 ('Dense deposit disease') Type 3
201
Q: What are the causes of Type 1 Membranoproliferative Glomerulonephritis?
Cryoglobulinaemia Hepatitis C
202
Q: What is seen on renal biopsy for Type 1 Membranoproliferative Glomerulonephritis?
Electron microscopy: Subendothelial and mesangium immune deposits of electron-dense material Resulting in a 'tram-track' appearance
203
Q: What are the causes of Type 2 Membranoproliferative Glomerulonephritis ('Dense deposit disease')?
Partial lipodystrophy (classically loss of subcutaneous tissue from the face) Factor H deficiency
204
Q: What causes Type 2 Membranoproliferative Glomerulonephritis ('Dense deposit disease')?
Persistent activation of the alternative complement pathway Low circulating levels of C3
205
Q: What is seen on renal biopsy for Type 2 Membranoproliferative Glomerulonephritis?
Electron microscopy: Intramembranous immune complex deposits with 'dense deposits'
206
Q: What are the causes of Type 3 Membranoproliferative Glomerulonephritis?
Hepatitis B Hepatitis C
207
Q: What is the management for Membranoproliferative Glomerulonephritis?
Steroids may be effective.
208
Q: How is the anion gap calculated?
(Na+ + K+) - (Cl- + HCO₃⁻)
209
Q: What is the normal range for the anion gap?
A: 10-18 mmol/L.
210
Q: What is normal anion gap metabolic acidosis also known as?
A: Hyperchloraemic metabolic acidosis.
211
Q: What are the two types of lactic acidosis?
Type A: Sepsis, shock, hypoxia, burns Type B: Metformin
212
Q: How does Minimal Change Disease most commonly present?
A: Nephrotic syndrome.
213
Q: What are some causes of Minimal Change Disease?
Drugs: NSAIDs, rifampicin Hodgkin's lymphoma, thymoma Infectious mononucleosis
214
Q: What are the features of Minimal Change Disease?
Nephrotic syndrome Normotension (hypertension is rare) Highly selective proteinuria (only intermediate-sized proteins like albumin and transferrin leak through) Renal biopsy: Normal glomeruli on light microscopy, fusion of podocytes and effacement of foot processes on electron microscopy
215
Q: What is the management for Minimal Change Disease?
Oral corticosteroids: Majority of cases (80%) are steroid-responsive Cyclophosphamide: Next step for steroid-resistant cases
216
Q: What is the prognosis for Minimal Change Disease?
Overall good prognosis 1/3 have just one episode 1/3 have infrequent relapses 1/3 have frequent relapses that stop before adulthood
217
Q: What are the three defining features of Nephrotic Syndrome?
Proteinuria (> 3g/24hr) Hypoalbuminaemia (< 30g/L) Oedema
218
Q: What are the primary causes of Nephrotic Syndrome?
Minimal change disease Focal segmental glomerulosclerosis (FSGS) Membranous nephropathy
219
Q: What are the secondary causes of Nephrotic Syndrome?
Diabetes mellitus Systemic lupus erythematosus (SLE) Amyloidosis Infections (e.g. HIV, hepatitis B and C) Drugs (e.g. NSAIDs, gold therapy)
220
Q: What is the pathophysiology of Nephrotic Syndrome?
Damage to the glomerular basement membrane and podocytes leads to increased permeability to proteins. Proteinuria causes hypoalbuminaemia and oedema due to reduced plasma oncotic pressure. Loss of antithrombin-III, proteins C and S, and a rise in fibrinogen predisposes to thrombosis. Loss of thyroxine-binding globulin lowers total thyroid hormone, but not free thyroxine levels.
221
Q: What are the initial investigations for Nephrotic Syndrome?
Urine dipstick: Proteinuria and check for microscopic haematuria Midstream urine (MSU): To exclude urinary tract infection Quantify proteinuria using an early morning urinary protein:creatinine ratio or albumin:creatinine ratio FBC and coagulation screen Urea and electrolytes
222
Q: What is the increased risk of thromboembolism in Nephrotic Syndrome associated with?
Loss of antithrombin III and plasminogen in the urine, which increases the risk of: Deep vein thrombosis Pulmonary embolism Renal vein thrombosis, leading to sudden deterioration in renal function.
223
Q: What is the connection between Nephrotic Syndrome and hyperlipidaemia?
Nephrotic syndrome can lead to hyperlipidaemia, which increases the risk of cardiovascular complications, including acute coronary syndrome and stroke.
224
Q: What increases the risk of infection in Nephrotic Syndrome?
Loss of urinary immunoglobulins, which impairs the immune system, making patients more susceptible to infections.
225
Q: How is contrast media nephrotoxicity defined?
A 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media. Contrast-induced nephropathy occurs 2-5 days after administration.
226
Q: What should be withheld in high-risk patients for contrast-induced nephropathy?
Metformin should be withheld for 48 hours and until renal function is normal due to the risk of lactic acidosis in the event of contrast-induced nephropathy.
227
Q: What is peritoneal dialysis (PD)?
A form of renal replacement therapy used as an alternative to haemodialysis. It is used as a stop-gap or for younger patients who prefer not to visit the hospital three times a week.
228
Q: What are common complications of peritoneal dialysis?
Peritonitis Sclerosing peritonitis
229
Q: What is the recommended antibiotic treatment for peritonitis in peritoneal dialysis patients?
The BNF recommends: Vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR Vancomycin added to dialysis fluid + ciprofloxacin by mouth. Aminoglycosides may be used for Gram-negative coverage instead of ceftazidime.
230
Q: What are the common causes of polyuria (occurring in >1 in 10 people)?
Diuretics, caffeine, & alcohol Diabetes mellitus Lithium Heart failure
231
Q: What are the infrequent causes of polyuria (occurring in 1 in 100 people)?
Hypercalcaemia Hyperthyroidism
232
Q: What are the rare causes of polyuria (occurring in 1 in 1000 people)?
Chronic renal failure Primary polydipsia Hypokalaemia
233
Q: What is a very rare cause of polyuria (occurring in <1 in 10,000 people)?
Diabetes insipidus
234
Q: When does Post-streptococcal glomerulonephritis typically occur after a group A beta-haemolytic Streptococcus infection?
7-14 days following infection, usually by Streptococcus pyogenes.
235
Q: What is the cause of Post-streptococcal glomerulonephritis?
Immune complex (IgG, IgM, and C3) deposition in the glomeruli.
236
Q: What are the general features of Post-streptococcal glomerulonephritis?
Headache Malaise Visible haematuria Proteinuria Oedema Hypertension Oliguria
237
Q: What blood test findings confirm Post-streptococcal glomerulonephritis?
Raised anti-streptolysin O titre (confirming recent streptococcal infection) Low C3 levels
238
Q: How do IgA nephropathy and Post-streptococcal glomerulonephritis differ in their renal biopsy features?
Post-streptococcal glomerulonephritis: Acute, diffuse proliferative glomerulonephritis Endothelial proliferation with neutrophils Electron microscopy: Subepithelial 'humps' from immune complex deposits Immunofluorescence: Granular or 'starry sky' appearance
239
Q: What is the defining feature of Rapidly Progressive Glomerulonephritis (RPGN)?
A rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli.
240
Q: What are the main causes of Rapidly Progressive Glomerulonephritis (RPGN)?
Goodpasture's syndrome Wegener's granulomatosis (now known as Granulomatosis with polyangiitis) SLE Microscopic polyangiitis
241
Q: What are the general features of Rapidly Progressive Glomerulonephritis (RPGN)?
Nephritic syndrome: Haematuria with red cell casts Proteinuria Hypertension Oliguria
242
Q: What features specific to the underlying cause can be seen in Rapidly Progressive Glomerulonephritis (RPGN)?
Goodpasture's syndrome: Haemoptysis Wegener's granulomatosis: Vasculitic rash or sinusitis
243
Q: What is the histological hallmark of Rapidly Progressive Glomerulonephritis (RPGN) on a renal biopsy?
The glomeruli are filled with crescents.
244
Q: What is the most common cause of Renal Artery Stenosis?
Atherosclerosis accounts for around 90% of cases.
245
Q: What are the main features of Renal Artery Stenosis (secondary to atherosclerosis)?
Hypertension Chronic kidney disease Flash pulmonary oedema
246
Q: What is renal papillary necrosis?
It describes coagulative necrosis of the renal papillae due to various causes.
247
Q: What are the common causes of renal papillary necrosis?
Severe acute pyelonephritis Diabetic nephropathy Obstructive nephropathy Analgesic nephropathy (previously due to phenacetin, now due to NSAIDs) Sickle cell anaemia
248
Q: What are the features of renal papillary necrosis?
Visible haematuria Loin pain Proteinuria
249
Q: What is the definition of renal failure?
Renal failure is defined as a glomerular filtration rate (GFR) of less than 15 ml/min.
250
Q: What are the types of renal replacement therapy (RRT)?
Haemodialysis Peritoneal dialysis Renal transplant
251
Q: What are the main features of haemodialysis?
Regular filtration of the blood through a dialysis machine in hospital Most patients need dialysis 3 times/week, lasting 3-5 hours per session Arteriovenous fistula created at least 8 weeks before treatment, most commonly in the lower arm Some patients may perform home haemodialysis
252
Q: What are the two types of peritoneal dialysis?
Continuous ambulatory peritoneal dialysis (CAPD): Exchanges last 30-40 minutes, with dwell times lasting 4-8 hours, and the patient may go about their normal activities. Automated peritoneal dialysis (APD): A dialysis machine fills and drains the abdomen while the patient sleeps, performing 3-5 exchanges over 8-10 hours each night.
253
Q: What are common complications of renal replacement therapy?
Haemodialysis: Site infection, endocarditis, hypotension, cardiac arrhythmia, back pain Peritoneal dialysis: Peritonitis, sclerosing peritonitis, catheter infection, constipation, hyperglycaemia Renal transplant: DVT/PE, opportunistic infections, malignancies, graft rejection, cardiovascular disease
254
Q: What is the life expectancy of a patient with renal failure who does not receive renal replacement therapy?
The average life expectancy is 6 months.
255
Q: What are the symptoms of renal failure that is not adequately managed with renal replacement therapy (RRT)?
Breathlessness, fatigue, insomnia, pruritus, poor appetite Swelling, weakness, weight gain/loss Abdominal cramps, nausea, muscle cramps Headaches, cognitive impairment, anxiety, depression Sexual dysfunction
256
Q: When matching for a renal transplant, which HLA antigens are most important?
The relative importance of the HLA antigens is: DR > B > A
257
Q: What are some post-op problems in renal transplantation?
Acute tubular necrosis (ATN) of graft Vascular thrombosis Urine leakage Urinary tract infection (UTI)
258
Q: What is hyperacute rejection in renal transplantation, and what is its cause?
Occurs minutes to hours after transplant Due to pre-existing antibodies against ABO or HLA antigens It is a Type II hypersensitivity reaction Leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the graft No treatment is possible, and the graft must be removed.
259
Q: What are the causes and features of acute graft failure?
Occurs < 6 months post-transplant Usually due to mismatched HLA, causing cell-mediated (cytotoxic T cells) rejection Typically asymptomatic but detected by a rising creatinine, pyuria, and proteinuria Other causes include cytomegalovirus (CMV) infection May be reversible with steroids and immunosuppressants.
260
Q: What are the causes of chronic graft failure?
Occurs > 6 months post-transplant Caused by both antibody and cell-mediated mechanisms, leading to fibrosis of the transplanted kidney (chronic allograft nephropathy) Recurrence of the original renal disease, with causes in the order of frequency: Minimal change glomerulonephritis (MCGN) IgA nephropathy Focal segmental glomerulosclerosis (FSGS)
261
Q: What is an example regime for renal transplant immunosuppression?
Initial regimen: Ciclosporin/Tacrolimus + Monoclonal antibody Maintenance regimen: Ciclosporin/Tacrolimus + Mycophenolate mofetil (MMF) or Sirolimus Steroids added if there are more than one steroid-responsive acute rejection episode.
262
Q: What are the common causes of rhabdomyolysis?
Seizure Collapse/coma (e.g., elderly patient found after 8 hours) Ecstasy Crush injury McArdle's syndrome Drugs (e.g., statins, especially when co-prescribed with clarithromycin)
263
Q: What are the features of rhabdomyolysis?
Acute kidney injury with disproportionately raised creatinine Elevated creatine kinase (CK): typically 5 times the upper limit of normal (elevations of 2-4 times normal are not supportive) Myoglobinuria: dark or reddish-brown urine Hypocalcaemia: myoglobin binds calcium Elevated phosphate: released from myocytes Hyperkalaemia: may develop before renal failure Metabolic acidosis
264
Q: How is rhabdomyolysis managed?
IV fluids to maintain good urine output Urinary alkalinization (sometimes used)
265
Q: What are the indications for spironolactone?
Ascites: in patients with cirrhosis and secondary hyperaldosteronism Hypertension: used as a step 4 treatment according to NICE guidelines Heart failure: shown to reduce all-cause mortality in the RALES study (for NYHA III and IV) Nephrotic syndrome Conn's syndrome
266
Q: What are the adverse effects of spironolactone?
Hyperkalaemia Gynaecomastia (less common with eplerenone)
267
Q: What is lupus nephritis?
A: Lupus nephritis is a severe manifestation of Systemic Lupus Erythematosus (SLE) that can lead to end-stage renal disease. It requires regular monitoring through urinalysis to detect proteinuria.
268
Q: What is the WHO classification for lupus nephritis?
Class I: Normal kidney Class II: Mesangial glomerulonephritis Class III: Focal (and segmental) proliferative glomerulonephritis Class IV: Diffuse proliferative glomerulonephritis Class V: Diffuse membranous glomerulonephritis Class VI: Sclerosing glomerulonephritis
269
Q: What are the characteristic renal biopsy findings in class IV lupus nephritis?
Endothelial and mesangial proliferation in the glomeruli 'Wire-loop' appearance of glomeruli Capillary wall thickening due to immune complex deposition (in severe cases) Electron microscopy shows subendothelial immune complex deposits Immunofluorescence shows a granular appearance
270
Q: What is the initial treatment for focal (class III) or diffuse (class IV) lupus nephritis?
Glucocorticoids Mycophenolate or cyclophosphamide for induction therapy
271
Q: What is the preferred treatment to reduce the risk of end-stage renal disease in lupus nephritis?
A: Mycophenolate is generally preferred over azathioprine for subsequent therapy to decrease the risk of developing end-stage renal disease.
272
Q: What do brown granular casts in urine indicate?
A: Brown granular casts are typically seen in acute tubular necrosis.
273
Q: What is the urine appearance in prerenal uraemia?
A: Prerenal uraemia usually presents with a 'bland' urinary sediment.
274
Q: What do red cell casts in urine suggest?
A: Red cell casts are indicative of nephritic syndrome.
275
Indications for dialysis
Indications for dialysis (refractory AEIOU) A acidosis (ph<7.1] E electrolyte derangement (refractory hyperkalaemia) I intoxication/ingestion (alcohol/salicylates/lithium) O overload of fluid (congestive cardiac failure) U uraemia (uraemia pericarditis or encephalopathy)
276
Hyaline casts in urine
seen in normal urine, after exercise, during fever or with loop diuretics
277
What suggests prerenal cause over ATN
high sodium good response to fluids
278
What should be given to patients with nephrotic syndrome to reduce risk of thromboembolism
LMWH
279
pneumonic for causes of raised anion gap met acidosis
in acidosis you see kussmaul breathing so the mnemonic is kussmal K - ketones u - uraemia s - sepsis s - salicylate m - methanol a - aldehyde l - lactic acidosis
280
nephrotic vs nephritic causes
Nephritic syndromes: HAEMATURIA and proteins - IgA nephropathy (shorter); happens 2-3 days after strep a infection - Post strep glomerulonephropathy (longer); happens 2-3 weeks after febrile illness/strep a. pts have htn - Rapid progressive glomerulonephropathy - GPA NephrOtic syndrome: prOteins - Minimal chnage disease: very common in chidlren - Membranous nephropathy
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What is the most common cause of peritonitis in peritoneal dialysis
staph epidermidis
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What are maintenance fluids for paeds
First 10 kg 100 ml/kg Second 10 kg 50 ml/kg Subsequent kg 20 ml/kg
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most common cause of nephrotic syndrome in children
minimal change disease
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What do the kidneys look like in HIV associated nephropathy
Large
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Maintenance fluids for adults
30ml/kg/day
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Cancer thats most likely after renal transplantation
squamous cell carcinoma of skin
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What should be monitored in HSP
Blood pressure and urinalysis
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'string of beads appearance'
fibromuscular dysplasia
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what is the most common site of thrombosis in nephrotic syndrome
renal vein
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what scan should you do for AKI with an unknown cause
renal US
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Q: What is the most common type of glomerulonephritis in adults and what is its typical presentation?
A: Membranous glomerulonephritis is the most common type of glomerulonephritis in adults, typically presenting with nephrotic syndrome or proteinuria.
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Q: What does a renal biopsy in membranous glomerulonephritis reveal on electron microscopy?
A: Electron microscopy shows thickened basement membrane with subepithelial electron-dense deposits, creating a 'spike and dome' appearance.
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Q: What are some common causes of membranous glomerulonephritis?
Idiopathic (due to anti-phospholipase A2 antibodies) Infections (e.g., hepatitis B, malaria, syphilis) Malignancy (e.g., prostate, lung, lymphoma, leukaemia) Drugs (e.g., gold, penicillamine, NSAIDs) Autoimmune diseases (e.g., SLE, thyroiditis, rheumatoid)
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Q: What is the first-line treatment for membranous glomerulonephritis to reduce proteinuria and improve prognosis?
A: ACE inhibitors or angiotensin II receptor blockers (ARBs) are first-line treatments to reduce proteinuria and improve prognosis.
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Q: What is the role of immunosuppression in the treatment of membranous glomerulonephritis?
A: Immunosuppression is used for patients with severe or progressive disease. Corticosteroids alone are not effective; a combination of corticosteroids and another agent, such as cyclophosphamide, is often used.
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Q: When should anticoagulation be considered in membranous glomerulonephritis?
A: Anticoagulation should be considered for high-risk patients due to the risk of thromboembolism.
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Q: What is the prognosis of membranous glomerulonephritis and the "rule of thirds"?
One-third of patients experience spontaneous remission. One-third remain proteinuric. One-third develop end-stage renal failure (ESRF).
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Q: What are some good prognostic features in membranous glomerulonephritis?
A: Good prognostic features include female sex, young age at presentation, and asymptomatic proteinuria of a modest degree at presentation.
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What drug can slow down CKD progression in ADPKD
tolvaptan
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Management of suspected AKI if 1 - prerenal cause suspected or 2 - post renal cause
pre renal cause - fluid challenge post renal cause - US
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Causes of focal segmental glomelurosclerosis
FSG is caused (mostly) by the 4H's - Huh? - idiopathic - Hurt kidney - secondary to other nephropathies - HIV - Heroin
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what is the diagnostic test for bladder cancer
flexible cystoscopy
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what is a common complication of nephrotic syndrome and what is done for it
venous thromboembolism - LMWH given
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