Renal Flashcards
Q: What are the causes of normal anion gap (hyperchloraemic) metabolic acidosis?
Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison’s disease
Q: What conditions are associated with a raised anion gap in metabolic acidosis?
Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol
Q: What causes metabolic alkalosis?
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.
Q: What are the causes of metabolic alkalosis?
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
Q: What are the common causes of respiratory acidosis?
COPD
Decompensation in other respiratory conditions (e.g. life-threatening asthma, pulmonary oedema)
Sedative drugs: benzodiazepines, opiate overdose
Q: What are the common causes of respiratory alkalosis?
Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
Altitude
Pregnancy
Q: What percentage of drug-induced acute kidney injury is accounted for by acute interstitial nephritis?
A: Acute interstitial nephritis accounts for 25% of drug-induced acute kidney injury.
Q: What are the common drug causes of acute interstitial nephritis?
Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide
Q: What systemic diseases can cause acute interstitial nephritis?
Systemic lupus erythematosus (SLE)
Sarcoidosis
Sjogren’s syndrome
Q: What infections can cause acute interstitial nephritis?
Hanta virus
Staphylococci
Q: What is seen in the histology of acute interstitial nephritis?
A: Marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules.
Q: What are the features of acute interstitial nephritis?
Fever
Rash
Arthralgia
Eosinophilia
Mild renal impairment
Hypertension
Q: What are the investigation findings in acute interstitial nephritis?
Sterile pyuria
White cell casts
Q: What are the symptoms of tubulointerstitial nephritis with uveitis (TINU)?
Fever
Weight loss
Painful, red eyes
Q: What is found on urinalysis in tubulointerstitial nephritis with uveitis (TINU)?
A: Urinalysis is positive for leukocytes and protein.
Q: What is one of the best ways to differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD)?
A: Renal ultrasound, as most patients with CKD have bilateral small kidneys.
Q: What are exceptions to the rule of bilateral small kidneys in CKD?
Autosomal dominant polycystic kidney disease
Diabetic nephropathy (early stages)
Amyloidosis
HIV-associated nephropathy
Q: What other feature suggests CKD rather than AKI?
A: Hypocalcaemia (due to lack of vitamin D).
Q: What does acute kidney injury (AKI) describe?
A: AKI describes a reduction in renal function following an insult to the kidneys.
Q: How are the causes of AKI traditionally divided?
A: Causes of AKI are divided into prerenal, intrinsic, and postrenal causes.
Q: What is a major cause of AKI?
A: Ischaemia (lack of blood flow) to the kidneys is a major cause of AKI.
Q: What are some examples of prerenal causes of AKI?
Hypovolaemia secondary to diarrhoea/vomiting
Renal artery stenosis
Q: What are some examples of intrinsic causes of AKI?
Glomerulonephritis
Acute tubular necrosis (ATN)
Acute interstitial nephritis (AIN)
Rhabdomyolysis
Tumour lysis syndrome
Q: What are some examples of postrenal causes of AKI?
Kidney stone in ureter or bladder
Benign prostatic hyperplasia
External compression of the ureter
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
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
Q: What are the key functions of the kidneys that are affected in AKI?
Fluid balance
Maintaining homeostasis (e.g., potassium, urea, creatinine balance)
Q: What are the key ways AKI may be detected?
Reduced urine output (oliguria)
Fluid overload
Rise in potassium, urea, or creatinine
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)
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)
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
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.
Q: Which medications are usually safe to continue in AKI?
Paracetamol
Warfarin
Statins
Aspirin (cardioprotective dose)
Clopidogrel
Beta-blockers
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
Q: How is hyperkalaemia treated in AKI?
Intravenous calcium gluconate
Combined insulin/dextrose infusion
Nebulised salbutamol
Calcium resonium (orally or enema)
Loop diuretics
Dialysis
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).
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
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
Q: How does prerenal uraemia and acute tubular necrosis (ATN) respond to a fluid challenge?
Prerenal uraemia: Good response
Acute tubular necrosis: Poor response
Q: What is the serum urea:creatinine ratio in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: Raised
Acute tubular necrosis: Normal
Q: What is the fractional urea excretion in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: < 35%
Acute tubular necrosis: > 35%
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
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
Q: What is the specific gravity of urine in prerenal uraemia compared to acute tubular necrosis (ATN)?
Prerenal uraemia: > 1020
Acute tubular necrosis: < 1010
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
Q: Why do the kidneys retain sodium in prerenal uraemia?
A: The kidneys hold on to sodium to preserve volume.
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
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
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
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
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
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)
Q: What is the most common inherited cause of kidney disease?
A: Autosomal Dominant Polycystic Kidney Disease (ADPKD).
Q: Which gene loci are associated with ADPKD?
A: PKD1 and PKD2, which code for polycystin-1 and polycystin-2, respectively.
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.
Q: What is the screening investigation for relatives of ADPKD patients?
A: Abdominal ultrasound.
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.
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.
Q: What are the findings in an ADPKD kidney on imaging?
A: Extensive cysts are seen in an enlarged kidney.
Q: What are the common renal features of ADPKD?
Hypertension
Recurrent UTIs
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones
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)
Q: What is the inheritance pattern of Alport’s syndrome?
A: Alport’s syndrome is usually inherited in an X-linked dominant pattern.
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).
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.
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.
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
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.
Q: What diagnostic tests are used to confirm Alport’s syndrome?
Molecular genetic testing
Renal biopsy
Electron microscopy (for basket-weave appearance)
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.
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).
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
Q: How is the anion gap calculated?
(Sodium + Potassium) - (Bicarbonate + Chloride)
Q: What is the normal range for the anion gap?
A: The normal anion gap is 8-14 mmol/L.
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
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)
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.
Q: What are the common features of Goodpasture’s syndrome?
Pulmonary hemorrhage
Rapidly progressive glomerulonephritis (acute kidney injury)
Nephritis → Proteinuria + Hematuria
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.
Q: What genetic association is linked to Goodpasture’s syndrome?
A: It is associated with HLA DR2.
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
Q: What is the main treatment for Goodpasture’s syndrome?
Plasma exchange (plasmapheresis)
Steroids
Cyclophosphamide
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
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.
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.
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.
Q: What other organ is typically involved in ARPKD?
A: Liver involvement is typical, such as portal and interlobular fibrosis.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
