Nephrology Flashcards
What are some of the drugs that need to be stopped in AKI as they may worsen renal function?
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od) • Aminoglycosides • ACE inhibitors • Angiotensin II receptor antagonists • Diuretics
May have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)
• Metformin
• Lithium
• Digoxin
What are the sympyomts and signs of AKI?
Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:
- Reduced urine output
- Pulmonary and peripheral oedema
- Arrhythmias (secondary to changes in potassium and acid-base balance)
- Features of uraemia (for example, pericarditis or encephalopathy)
Pre-renal causes of AKI?
- Hypovolaemia (diarrhoea/vomiting)
- Renal artery stenosis
Intrinsic causes of AKI?
- Glomerulonephritis
- Acute tubular necrosis (ATN)
- Acute interstitial nephritis (AIN), respectively
- Rhabdomyolysis
- Tumour lysis syndrome
Post-renal causes of AKI?
- Kidney stone in ureter or bladder
- Benign prostatic hyperplasia
- External compression of the ureter
Reduced urine output or oliguria is defined as a urine output of less than ….?
Oliguria is defined as a urine output of less than 0.5 ml/kg/hour
What are the features of rhabdomyolysis?
- AKI with disproportionately raised creatinine
- Elevated creatine kinase (CK)
- Myoglobinuria
- hypocalcaemia (myoglobin binds calcium)
- elevated phosphate (released from myocytes)
- Hyperkalaemia (may develop before renal failure)
- metabolic acidosis
What kind of rash is seen in Henoch-Schonlein purpura?
Palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
What are the symptoms of Henoch-Schonlein purpura?
- Palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
- Abdominal pain
- Polyarthritis
- Features of IgA nephropathy may occur e.g. haematuria, renal failure
HSP is usually seen in children following an infection.
What is the formula for measuring anion gap?
[(Na+) + (K+)] - [(Cl) + (HCO3)]
What are the causes of high anion gap metabolic acidosis?
If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids:
- Lactic acid (sepsis, shock, tissue ischaemia)
- Urate (renal failure)
- Ketones (diabetic ketoacidosis, alcohol)
- Drugs/ toxins (salicylates, methanol, ethylene glycol)
MUD PILES
Methanol Uremia Diabetic ketoacidosis Paraldehyde Iron/Isoniazid Lactic acidosis (ex: in sepsis due to hypoperfusion) Ethylene glycol Salicylate
What are the causes of normal anion gap metabolic acidosis?
If there is a metabolic acidosis with a normal anion gap, then this is either due to loss of bicarbonate, or accumulation of H+ ions = hyperchloraemic metabolic acidosis
- Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
- Renal tubular acidosis
- Drugs: e.g. acetazolamide
- Ammonium chloride injection
- Addison’s disease
How is the requirement for maintenance fluids calculated for patients?
NICE recommend the following for maintenance fluids:
-25-30 ml/kg/day of water
Example: a 80kg patient, for a 24 hour period
80 x 25 = 2000
2 litres of water
How is paediatric maintenance fluids calculated?
VOLUME PER DAY (over 24 hours)
First 10 kg 100ml/kg/day
Next 10 kg 50ml/kg/day
>= 20.1 kg 20ml/kg/day
Hourly RATE (4-2-1 Rule)
4ml/kg/hour
2ml/kg/hour
1ml/kg/hour
What is the preferred method of access for haemodialysis?
Arteriovenous fistulas
Arteriovenous fistulas are direct connections between arteries and veins. They may occur pathologically but are generally formed surgically to allow access for haemodialysis. The time taken for an arteriovenous fistula to develop is 6 to 8 weeks.
The high blood flow from the artery through the vein allows the fistula to grow larger and stronger. A healthy AV fistula has:
A bruit (a rumbling sound that you can hear) A thrill (a rumbling sensation that you can feel) Good blood flow rate
Changes in the bruit or thrill at the fistula site may indicate stenosis.
What are possible complications of AV fistulas?
- Infection
- Thrombosis
may be detected by the absence of a bruit - Stenosis
may present with acute limb pain - Steal syndrome
ischaemia
How is CKD staged?
CKD may be classified according to GFR:
CKD stage
1 : Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2: 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a: 45-59 ml/min, a moderate reduction in kidney function
3b: 30-44 ml/min, a moderate reduction in kidney function
4: 15-29 ml/min, a severe reduction in kidney function
5: Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
What are the symptoms of diabetes insipidus?
Polyuria
Polydipsia
What are the investigations performed in diabetes insipidus?
- High plasma osmolality, low urine osmolality
- a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
- Water deprivation test
What are the causes of nephrogenic diabetes insipidus?
Diabetes insipidus (DI) is a condition characterised by either a deficiency of antidiuretic hormone, ADH, (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
Causes of nephrogenic DI:
- Genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
- Electrolytes: hypercalcaemia, hypokalaemia
- Drugs: demeclocycline, lithium
- Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
What are the causes of cranial diabetes insipidus?
Diabetes insipidus is a condition characterised by either a deficiency of ADH, (cranial DI) or an insensitivity to ADH (nephrogenic DI).
Causes of cranial DI:
- Idiopathic
- Post head injury
- Pituitary surgery
- Craniopharyngiomas
- Histiocytosis X
- DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
- Haemochromatosis
What are the causes of non-visible haematuria?
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
What is an important step in reducing the risk of contrast-induced nephropathy?
Intravenous 0.9% Sodium chloride, pre- and post- procedure
What is the time limit for acute graft rejection and chronic graft rejection?
Acute graft failure (< 6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants
Causes of chronic graft failure (> 6 months)
both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)
What is the commonest cause of nephrotic syndrome in children?
Minimal change glomerulonephritis (causes 80% in children, 30% in adults)
Nephrotic Syndrome symptoms?
Triad of:
- Proteinuria (> 3g/24hr) causing
- Hypoalbuminaemia (< 30g/L) and
- Oedema
Management of minimal change glomerulonephritis?
Management:
- Majority of cases (80%) are STEROID-responsive
cyclophosphamide is the next step for steroid-resistant cases
Prognosis is overall good, although relapse is common. Roughly:
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
What are the causes of CKD?
Diabetic nephropathy Chronic glomerulonephritis Chronic pyelonephritis Hypertension Adult polycystic kidney disease
Causes of metabolic alkalosis?
- vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)
- diuretics
- liquorice, carbenoxolone
- hypokalaemia
- primary hyperaldosteronism
- Cushing’s syndrome
- Bartter’s syndrome
- congenital adrenal hyperplasia
Causes of respiratory acidosis?
- COPD
- decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema
- sedative drugs: benzodiazepines, opiate overdose
Causes of respiratory alkalosis?
- Anxiety leading to hyperventilation
- pulmonary embolism
- salicylate poisoning
- CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
- altitude
- pregnancy
What is the commonest cause of glomerulonephritis?
IgA nephropathy (also known as Berger’s disease) is the commonest cause of glomerulonephritis worldwide. It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.
How do you differentiate between IgA nephropathy and post streptococcal glomerulonephritis?
- Post-streptococcal glomerulonephritis is associated with low complement levels
- Main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
- IgA nephropathy usually develops 1 - 2 days after URTI. Post streptococcal glomerulonephritis usually develops 1 - 2 weeks after URTI.
What is the most appropriate screening test for AD polycystic kidney disease?
Ultrasound is the screening investigation for relatives for adult polycystic kidney disease. (not genetic testing)
What is the treatment for cranial DI?
Desmopressin!
Cranial DI essentially means the body is unable to produce sufficient amounts of vasopressin a.k.a antidiuretic hormone (ADH). This is can be treated with synthetic forms of vasopressin such as desmopressin.
What is the treatment for nephrogenic DI?
Thiazides (ex: chlorothiazide), low salt/protein diet
Nephrogenic DI is caused by the kidneys inability to respond to vasopressin. This means giving a patient synthetic vasopressin will be ineffective. It may seem paradoxical that a thiazide diuretic would be a treatment for this condition as polyuria is a symptom of the disorder.
DI leads to the production of vast amounts of dilute urine which is dehydrating and raises the plasma osmolarity, stimulating thirst. The effect of the thiazide causes more sodium to be released into the urine. This lowers the serum osmolarity which helps to break the polyuria-polydipsia cycle.
Features of ADPKD?
- Hypertension
- Recurrent UTIs
- Abdominal pain
- Renal stones
- Haematuria
- Chronic kidney disease
What are the extra-renal manifestations of ADPKD?
- Liver cysts (70%): may cause hepatomegaly
- Berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
- Cardiovascular system: aortic root dilation, aortic dissection mitral valve prolapse, mitral/tricuspid incompetence
- Cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
