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.
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.
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).
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.
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.
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)
Q: How is chronic kidney disease (CKD) usually diagnosed?
A: CKD is usually asymptomatic and is diagnosed following abnormal urea and electrolyte results.
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
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).
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.
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.
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.
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)
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.
Q: What is the first-line management for mineral bone disease in CKD?
Reduced dietary phosphate intake
Phosphate binders
Vitamin D (alfacalcidol, calcitriol)
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.
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.
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.
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.
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.
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)
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
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.
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.
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.
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
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
Q: What are the main clinical features of diabetes insipidus?
Polyuria (excessive urination)
Polydipsia (excessive thirst)
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.
Q: What is the management for nephrogenic diabetes insipidus?
Thiazide diuretics
Low salt/protein diet
Q: How is central diabetes insipidus treated?
Desmopressin (synthetic ADH)
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.
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
Q: What is the target blood pressure for managing diabetic nephropathy?
< 130/80 mmHg
Q: When should ACE inhibitors or angiotensin-II receptor antagonists be started in diabetic nephropathy management?
When urinary ACR is ≥ 3 mg/mmol.
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.
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.
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
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
Q: How does darbepoetin differ from erythropoietin?
Darbepoetin carries a reduced risk of pure red cell aplasia compared to erythropoietin.
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.
Q: What are the main features of Fanconi syndrome?
Type 2 (proximal) renal tubular acidosis
Polyuria
Aminoaciduria
Glycosuria
Phosphaturia
Osteomalacia (due to phosphate loss)
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
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%.
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)
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
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
Q: What is a potential complication of using 0.9% saline for large volumes of fluid replacement?
Increased risk of hyperchloraemic metabolic acidosis.
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.
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
Q: Why is Focal Segmental Glomerulosclerosis noted to have a high recurrence rate?
FSGS has a high recurrence rate in renal transplants.
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
Q: What is the management for Focal Segmental Glomerulosclerosis (FSGS)?
Steroids ± immunosuppressants.
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
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
Q: What are the spurious causes of red/orange urine that are not due to blood?
Foods: Beetroot, rhubarb
Drugs: Rifampicin, doxorubicin
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.
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.
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.
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.
Q: What is the classic triad of Haemolytic Uraemic Syndrome (HUS)?
Acute kidney injury
Microangiopathic haemolytic anaemia (MAHA)
Thrombocytopenia
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.
Q: What are some other causes of secondary HUS besides STEC infection?
Pneumococcal infection
HIV
Rare causes:
Systemic lupus erythematosus (SLE)
Drugs
Cancer
Q: What is primary (atypical) HUS caused by?
Complement dysregulation.
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.
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
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.
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).
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
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
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).
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.
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
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.
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
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
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
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
Q: What are the features of hypokalaemia?
Muscle weakness
Hypotonia
Predisposition to digoxin toxicity (especially in patients on diuretics)
Q: What ECG features are associated with hypokalaemia?
U waves
Small or absent T waves
Prolonged PR interval
ST depression
Q: What is IgA nephropathy also known as?
A: Berger’s disease.
Q: What is the commonest cause of glomerulonephritis worldwide?
A: IgA nephropathy (Berger’s disease).
Q: What are some associated conditions with IgA nephropathy?
Alcoholic cirrhosis
Coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura
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).
Q: What are the histological features of IgA nephropathy?
Mesangial hypercellularity
Positive immunofluorescence for IgA and C3
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
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.
Q: What is the initial treatment for persistent proteinuria in IgA nephropathy?
ACE inhibitors.
Q: What should be done if there is active disease or failure to respond to ACE inhibitors in IgA nephropathy?
Immunosuppression with corticosteroids.
Q: How does Membranoproliferative Glomerulonephritis typically present?
Nephrotic syndrome
Haematuria
Proteinuria
Q: What are the types of Membranoproliferative Glomerulonephritis?
Type 1
Type 2 (‘Dense deposit disease’)
Type 3
Q: What are the causes of Type 1 Membranoproliferative Glomerulonephritis?
Cryoglobulinaemia
Hepatitis C
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
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
Q: What causes Type 2 Membranoproliferative Glomerulonephritis (‘Dense deposit disease’)?
Persistent activation of the alternative complement pathway
Low circulating levels of C3
Q: What is seen on renal biopsy for Type 2 Membranoproliferative Glomerulonephritis?
Electron microscopy: Intramembranous immune complex deposits with ‘dense deposits’
Q: What are the causes of Type 3 Membranoproliferative Glomerulonephritis?
Hepatitis B
Hepatitis C
Q: What is the management for Membranoproliferative Glomerulonephritis?
Steroids may be effective.
Q: How is the anion gap calculated?
(Na+ + K+) - (Cl- + HCO₃⁻)
Q: What is the normal range for the anion gap?
A: 10-18 mmol/L.
Q: What is normal anion gap metabolic acidosis also known as?
A: Hyperchloraemic metabolic acidosis.
Q: What are the two types of lactic acidosis?
Type A: Sepsis, shock, hypoxia, burns
Type B: Metformin
Q: How does Minimal Change Disease most commonly present?
A: Nephrotic syndrome.
Q: What are some causes of Minimal Change Disease?
Drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
Infectious mononucleosis
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
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
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
Q: What are the three defining features of Nephrotic Syndrome?
Proteinuria (> 3g/24hr)
Hypoalbuminaemia (< 30g/L)
Oedema
Q: What are the primary causes of Nephrotic Syndrome?
Minimal change disease
Focal segmental glomerulosclerosis (FSGS)
Membranous nephropathy
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)
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.
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
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.
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.
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.
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.
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.
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.
Q: What are common complications of peritoneal dialysis?
Peritonitis
Sclerosing peritonitis
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.
Q: What are the common causes of polyuria (occurring in >1 in 10 people)?
Diuretics, caffeine, & alcohol
Diabetes mellitus
Lithium
Heart failure
Q: What are the infrequent causes of polyuria (occurring in 1 in 100 people)?
Hypercalcaemia
Hyperthyroidism
Q: What are the rare causes of polyuria (occurring in 1 in 1000 people)?
Chronic renal failure
Primary polydipsia
Hypokalaemia
Q: What is a very rare cause of polyuria (occurring in <1 in 10,000 people)?
Diabetes insipidus
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.
Q: What is the cause of Post-streptococcal glomerulonephritis?
Immune complex (IgG, IgM, and C3) deposition in the glomeruli.
Q: What are the general features of Post-streptococcal glomerulonephritis?
Headache
Malaise
Visible haematuria
Proteinuria
Oedema
Hypertension
Oliguria
Q: What blood test findings confirm Post-streptococcal glomerulonephritis?
Raised anti-streptolysin O titre (confirming recent streptococcal infection)
Low C3 levels
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
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.
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
Q: What are the general features of Rapidly Progressive Glomerulonephritis (RPGN)?
Nephritic syndrome:
Haematuria with red cell casts
Proteinuria
Hypertension
Oliguria
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
Q: What is the histological hallmark of Rapidly Progressive Glomerulonephritis (RPGN) on a renal biopsy?
The glomeruli are filled with crescents.
Q: What is the most common cause of Renal Artery Stenosis?
Atherosclerosis accounts for around 90% of cases.
Q: What are the main features of Renal Artery Stenosis (secondary to atherosclerosis)?
Hypertension
Chronic kidney disease
Flash pulmonary oedema
Q: What is renal papillary necrosis?
It describes coagulative necrosis of the renal papillae due to various causes.
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
Q: What are the features of renal papillary necrosis?
Visible haematuria
Loin pain
Proteinuria
Q: What is the definition of renal failure?
Renal failure is defined as a glomerular filtration rate (GFR) of less than 15 ml/min.
Q: What are the types of renal replacement therapy (RRT)?
Haemodialysis
Peritoneal dialysis
Renal transplant
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
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.
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
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.
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
Q: When matching for a renal transplant, which HLA antigens are most important?
The relative importance of the HLA antigens is:
DR > B > A
Q: What are some post-op problems in renal transplantation?
Acute tubular necrosis (ATN) of graft
Vascular thrombosis
Urine leakage
Urinary tract infection (UTI)
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.
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.
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)
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.
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)
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
Q: How is rhabdomyolysis managed?
IV fluids to maintain good urine output
Urinary alkalinization (sometimes used)
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
Q: What are the adverse effects of spironolactone?
Hyperkalaemia
Gynaecomastia (less common with eplerenone)
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.
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
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
Q: What is the initial treatment for focal (class III) or diffuse (class IV) lupus nephritis?
Glucocorticoids
Mycophenolate or cyclophosphamide for induction therapy
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.
Q: What do brown granular casts in urine indicate?
A: Brown granular casts are typically seen in acute tubular necrosis.
Q: What is the urine appearance in prerenal uraemia?
A: Prerenal uraemia usually presents with a ‘bland’ urinary sediment.
Q: What do red cell casts in urine suggest?
A: Red cell casts are indicative of nephritic syndrome.
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)
Hyaline casts in urine
seen in normal urine, after exercise, during fever or with loop diuretics
What suggests prerenal cause over ATN
high sodium
good response to fluids
What should be given to patients with nephrotic syndrome to reduce risk of thromboembolism
LMWH
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
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
What is the most common cause of peritonitis in peritoneal dialysis
staph epidermidis
What are maintenance fluids for paeds
First 10 kg 100 ml/kg
Second 10 kg 50 ml/kg
Subsequent kg 20 ml/kg
most common cause of nephrotic syndrome in children
minimal change disease
What do the kidneys look like in HIV associated nephropathy
Large
Maintenance fluids for adults
30ml/kg/day
Cancer thats most likely after renal transplantation
squamous cell carcinoma of skin
What should be monitored in HSP
Blood pressure and urinalysis
‘string of beads appearance’
fibromuscular dysplasia
what is the most common site of thrombosis in nephrotic syndrome
renal vein
what scan should you do for AKI with an unknown cause
renal US
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.
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.
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)
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.
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.
Q: When should anticoagulation be considered in membranous glomerulonephritis?
A: Anticoagulation should be considered for high-risk patients due to the risk of thromboembolism.
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).
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.
What drug can slow down CKD progression in ADPKD
tolvaptan
Management of suspected AKI if 1 - prerenal cause suspected or 2 - post renal cause
pre renal cause - fluid challenge
post renal cause - US
Causes of focal segmental glomelurosclerosis
FSG is caused (mostly) by the 4H’s
- Huh? - idiopathic
- Hurt kidney - secondary to other nephropathies
- HIV
- Heroin
what is the diagnostic test for bladder cancer
flexible cystoscopy
what is a common complication of nephrotic syndrome and what is done for it
venous thromboembolism - LMWH given
