Renal and Urology Flashcards
What is AKI and what are the NICE guidelines for what qualifies as AKI?
A rapid drop in kidney function
Increased creatinine > 26micromol/L in 48hrs
Increased creatinine > 50% in 7 days
Urine output <0.5 ml/kg/hr over 6hrs (Oliguria)
What are the risk factors for AKI?
> 65 years
Sepsis
CKD
HF
Diabetes
Liver disease
Cognitive impairment (leading to reduced fluid intake)
Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
Radiocontrast agents (e.g., used during CT scans
What are the pre-renal causes of AKI?
Pre-renal (most common):
Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood
Dehydration
Shock (e.g., sepsis or acute blood loss)
Heart failure
Urine osmolality high, urine sodium low
What are the renal causes of AKI?
Renal causes:
Intrinsic disease in the kidney
Acute tubular necrosis (most common)
Glomerulonephritis
Acute interstitial nephritis
Haemolytic uraemic syndrome
Rhabdomyolysis
What are the post-renal causes of AKI?
Post-renal:
Obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function (Obstructive uropathy)
Kidney stones
Tumours (e.g., retroperitoneal, bladder or prostate)
Strictures of the ureters or urethra
Benign prostatic hyperplasia (benign enlarged prostate)
Neurogenic bladder
What is acute tubular necrosis?
Necrosis of the epithelial cells of the renal tubules due to:
- Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
- Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)
granular, muddy brown casts on urinalysis
Cells regenerate 1-3 weeks therefore reversible
What is Acute Interstitial Nephritis? What are its features and management?
Acute inflammation of the interstitium caused by:
Drugs (NSAIDs,penicillin, rifampicin, allopurinol, furosemide)
Infections (E. coli or HIV)
Autoimmune conditions (sarcoidosis or SLE, Sjorgens syndrome)
Features:
Impaired renal function
‘allergic’ type picture (raised urinary WCC and eosinophils),
Rash
Fever
Flank pain
Eosinophilia
Treat underlying cause. Steroids may reduce inflammation and improve recovery
What are the investigations for AKI?
U&Es
Urinalysis assesses for protein, blood, leucocytes, nitrites and glucose:
Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes
Ultrasound of the urinary tract assesses for obstruction when a post-renal cause is suspected.
What is the management for AKI?
Reverse underlying cause:
IV fluids for dehydration and hypovolemia
Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
Dialysis may be required in severe cases
What are some complications of AKI?
Fluid overload, heart failure and pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia can cause encephalopathy and pericarditis
What differs in U&Es between acute tubular necrosis and prerenal uraemia?
Prerenal uraemia - kidneys hold on to sodium to preserve volume
What are the staging criteria for AKI?
Stage 1:
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
Stage 2:
Increase in creatinine to 2.0 to 2.9 times baseline
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3
Increase in creatinine to ≥ 3.0 times baseline
Increase in creatinine to ≥353.6 µmol/L
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours
The initiation of kidney replacement therapy
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
When should you refer AKI 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
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
What is CKD and what are some causes?
Chronic reduction in kidney function sustained over 3 months. It tends to be permanent and progressive
(<60 mL/min/1.73m² for ≥3 months) and/or kidney damage (proteinuria, haematuria).
Diabetes
Hypertension
Medications (e.g., NSAIDs or lithium)
Glomerulonephritis
Chronic Pylenophritis
Polycystic kidney disease
What is the presentation of CKD
Most are asymptomatic. Can present with:
Fatigue
Pallor (due to anaemia)
Foamy urine (proteinuria)
Nausea
Loss of appetite
Pruritus (itching)
Oedema
Hypertension
Peripheral neuropathy
What are investigations for CKD?
eGFR below 60 mL/min/1.73 m2 for 3 months
Proteinuria (ACR) above 3 mg/mmol for 3 months
Haematuria (Urine Dipstick)
Renal Ultrasound
BP
HbA1c
Lipid profile
What is the classification of CKD?
G1, eGFR >90 A1, ACR< 3 mg/mmol
G2, eGFR 60-89 A2, ACR 3-30 mg/mmol
G3a eGFR 45-59 A3, ACR > 30 mg/mmol
G3b eGFR 30-44
G4, eGFR 15-29
G5, eGFR < 15
What is accelerated progression CKD
A sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73m2
What are some complications of CKD?
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
End-stage kidney disease
Dialysis-related complications
When should you refer for CKD?
eGFR < 30 mL/min
Urine ACR > 70 mg/mmol
Accelerated progression
5-year risk of requiring dialysis over 5%
Uncontrolled hypertension despite 4 or more antihypertensives
What can you do to treat the underlying cause of CKD?
Optimising diabetic control
Optimising hypertension control
Reducing or avoiding nephrotoxic drugs
Treating glomerulonephritis
How can you manage BP in CKD?
BP target is 130/80 ( <80yrs) and ACR> 70
ACE inhibitors (or angiotensin II receptor blockers)
SGLT-2 inhibitors (specifically dapagliflozin)
Furosemide for fuid overload
EPO for anaemia related to CKD
Renal replacement therapy (RRT): Dialysis or kidney transplant when GFR is below 15 mL/min/1.73m² or when complications (e.g., uraemia, hyperkalaemia) develop.
What medication is prescribed to all patients with CKD for CVD risk?
Atorvastatin
When are ACE inhibitors offered for hypertension in CKD?
Diabetes plus a urine ACR above 3 mg/mmol
Hypertension plus a urine ACR above 30 mg/mmol
All patients with a urine ACR above 70 mg/mmol
When are SGLT2 Inhibitors offered for hypertension in CKD?
Offered to patients with:
- Diabetes plus a urine ACR above 30 mg/mmol
Considered for patients with:
- Diabetes plus a urine ACR or 3-30 mg/mmol
- Non-diabetics with an ACR of 22.6 mg/mmol or above
How is anaemia of CKD treated?
Oral Iron for 3 months
if the target not reached, IV iron
EPO
What are the features of renal bone disease?
Chronic kidney disease-mineral and bone disorder (CKD-MBD)
High serum phosphate
Low vitamin D activity
Low serum calcium
What is the management of CKD-MBD?
Reduced dietary intake of phosphate is recommended
First-line:
- Phosphate binders (sevelamer)
- Vitamin D: alfacalcidol, calcitriol
- Parathyroidectomy
What is Autosomal dominant polycystic kidney disease (ADPKD)
A genetic condition where the healthy kidney tissue is replaced with many fluid-filled cysts.
The most common inherited cause of CKD (PKD1 and PKD2)
What are the diagnostic criteria for ADPKD?
Ultrasound diagnostic criteria:
2 cysts, unilateral or bilateral, if aged < 30 years
2 cysts in both kidneys if aged 30-59 years
4 cysts in both kidneys if aged > 60 years
CT/MRI: For more detailed imaging, especially in patients with equivocal ultrasound findings.
Genetic testing: In some cases, to confirm ADPKD in asymptomatic individuals.
What are some symptoms of ADPKD?
Hypertension (early sign due to cyst enlargement).
Abdominal pain from cysts pressing on surrounding structures.
Haematuria (from cyst rupture or bleeding).
Chronic kidney disease with progression to end-stage renal failure in adulthood.
What is the treatment for ADPKD?
Antihypertensives for hypertension (e.g., ACE inhibitors)
Analgesia for acute pain
Antibiotics for infections (e.g., UTIs or cyst infections)
Drainage of symptomatic can be performed by aspiration or surgery
Dialysis for end-stage renal failure
Renal transplant for end-stage renal failure
Tolvaptan (vasopressin receptor 2 antagonist if:
CKD G2/3 at the start of treatment
Rapidly progressing CKD
What external factors can affect the result of eGFR?
Pregnancy
Muscle mass (e.g. amputees, body-builders)
Eating red meat 12 hours before the sample being taken
What are the modifiable and non-modifiable risk factors of diabetic nephropathy?
Modifiable
Hypertension
Hyperlipidaemia
Smoking
Poor glycaemic control
Raised dietary protein
Non-modifiable:
Male sex
Duration of diabetes
Genetic predisposition (e.g. ACE gene polymorphisms)
What is the management of diabetic nephropathy?
Screened annually using ACR
should be an early morning specimen
ACR > 2.5 = microalbuminuria
Management
Dietary protein restriction
Blood glucose control: Tight control with insulin or oral hypoglycaemics (e.g., Metformin, SGLT2 inhibitors like Empagliflozin, which may also slow progression of kidney disease).
Blood pressure control: Aim for < 130/80 mmHg, ACE inhibitors (e.g., Ramipril, Lisinopril) or ARBs (e.g., Losartan, Irbesartan) are first-line to reduce proteinuria and slow kidney function decline. If urinary ACR of 3 mg/mmol or more
Statins: Atorvastatin for cardiovascular protection.
Diuretics: To manage fluid retention.
Renal replacement therapy: In end-stage renal disease (ESRD), consider dialysis or kidney transplant.
What are the stages of diabetic nephropathy?
Stage 1
- Hyperfiltration: increase in GFR,
may be reversible
Stage 2 (silent or latent phase)
- Most patients do not develop microalbuminuria for 10 years
GFR remains elevated
Stage 3 (incipient nephropathy)
- Microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)
Stage 4 (overt nephropathy)
- Persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)
- Hypertension
- Histology shows Kimmelstiel-Wilson nodules
Stage 5
- ESRD, GFR typically < 10ml/min
- Renal replacement therapy needed
What is Diabetes Inspidius?
Decreased secretion of ADH from the pituitary (cranial DI)
OR
Insensitivity to ADH (nephrogenic DI).
What are some causes of cranial DI?
Idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
Wolframs syndrome/ DIDMOAD (association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness)
haemochromatosis
What are some causes of nephrogenic DI?
genetic:
more common form affects the vasopressin (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes:
hypercalcaemia
hypokalemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulointerstitial disease: obstruction, sickle-cell, pyelonephritis
What are the features of DI? What investigation would you do and what would you see?
polyuria
polydipsia
Investigation
- Urine osmolality: Very low (hypotonic) urine in the face of hypernatremia (>700 mOsm/kg excludes DI)
- Plasma osmolality: Elevated, due to fluid loss.
- Water deprivation test: To differentiate between central and nephrogenic DI.
- Desmopressin (DDAVP) test: Central DI will respond to DDAVP with a significant reduction in urine output.
- MRI: For imaging the pituitary gland to identify structural abnormalities in central DI.
What is the management of DI?
- Central DI:
Desmopressin - Nephrogenic DI:
Low salt/protein diet
Thiazide diuretics (e.g., Hydrochlorothiazide) to reduce urine output.
Indomethacin (NSAID) may be added to enhance the effect of thiazides.
Amiloride may be used for lithium-induced nephrogenic DI to decrease renal resistance to ADH. - Fluid management: Ensure adequate water intake to prevent dehydration, particularly in hot weather or when ill.
What is Rhabdomyolysis?
Skeletal muscle breaking down and releasing:
Myoglobin
Potassium
Phosphate
Creatine kinase
What are some causes of Rhabdomyolysis?
Prolonged immobility, particularly frail patients who fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit)
Crush injuries
Seizures
Statins
What are the signs and symptoms of Rhabdomyolysis?
- Muscle pain, weakness, and swelling.
- Dark (tea-coloured) urine due to myoglobinuria.
- Reduced urine output (oliguria)
- Elevated creatine kinase (CK), lactate dehydrogenase (LDH), and serum potassium.
- Fever, nausea, and confusion in severe cases
- Fatigue
What are the investigations for Rhabdomyolysis?
CK: < 150 usually, elevated to 1000-100000, higher = increased risk of kidney injury
Urine dipstick (myoglobinuria)
U&E shows AKI and increased K+
ECG can show increased K+
What is the management for Rhabdomyolysis?
IV fluids
IV sodium bicarbonate (to increase urinary pH and reduce the toxic effects of myoglobinuria)
IV mannitol (to increase urine output and reduce oedema
Avoid nephrotoxic agents: Stop medications that may worsen renal function, such as NSAIDs and statins.
What are the 3 features of nephrotic syndrome?
- Proteinuria (> 3g/24hr) causing
- Hypoalbuminaemia (< 30g/L) and
- Oedema
What are the primary causes of nephrotic syndrome?
Minimal change disease
Focal segmental glomerulosclerosis (FSGS)
Membranous nephropathy
What are the secondary causes of nephrotic syndrome?
Diabetes mellitus
Systemic lupus erythematosus (SLE),
Amyloidosis
Infections (HIV, hepatitis B and C),
Drugs (NSAIDs, gold therapy)
What is the pathophysiology of nephrotic syndrome?
Damage to the glomerular basement membrane and podocytes leads to increased protein permeability.
This proteinuria results in hypoalbuminaemia and subsequent oedema due to reduced plasma oncotic pressure
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis
Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.
What are the investigations for nephrotic syndrome?
Urine dipstick: proteinuria and check for microscopic haematuria
MSU to exclude UTI
Quantify proteinuria using an early morning urinary protein: creatinine ratio or albumin: creatinine ratio
FBC and coagulation screen
U&Es
What are some complications of nephrotic syndrome?
Risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
- DVT, PE
- Renal vein thrombosis, resulting in a sudden deterioration in renal function
Hyperlipidaemia
increasing risk of ACS, stroke etc
CKD
Infection due to urinary immunoglobulin loss
Hypocalcaemia (vitamin D and binding protein lost in urine)
What are the features of minimal change disease?
Nephrotic syndrome
Normotension - hypertension is rare
Highly selective proteinuria
- only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus
Renal biopsy
- normal glomeruli on light microscopy
- electron microscopy shows the fusion of podocytes and effacement of foot processes
What is the management of minimal change disease?
Oral corticosteroids: 80% are steroid-responsive
Cyclophosphamide for steroid-resistant cases
What are the causes of FSGS?
Idiopathic
Secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
Heroin
Alport’s syndrome
Sickle-cell
What is the management of FSGS?
Steroids +/- Immunosuppressants
What is membranous glomerulonephritis?
Most common type of glomerulonephritis in adults and is the third most common cause of end-stage renal failure (ESRF). It usually presents with nephrotic syndrome or proteinuria.
Renal biopsy demonstrates:
electron microscopy: the basement membrane is thickened with subepithelial electron-dense deposits. This creates a ‘spike and dome’ appearance
What are some causes of membranous glomerulonephritis?
Idiopathic: due to anti-phospholipase A2 antibodies
Infections: hepatitis B, malaria, syphilis
Malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
Drugs: gold, penicillamine, NSAIDs
Autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
