Renal Flashcards
What rise in creatinine for criteria for AKI?
> 25 micromol/L in 48 hours
50% in 7 days
What urine output for criteria for AKI?
<0.5ml/kg/hr for > 6 hours
What are some pre-renal causes for AKI?
Inadequate blood supply
- Dehydration
- Hypotension
- Heart failure
What are some renal causes of AKI?
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
What are some post-renal causes of AKI?
Obstruction causing back pressure and reduced kidney function
- Kidney stones
- Masses such as cancer in the abdomen or pelvis
- Ureter or ureteral stictures
- Enlarged prostate or prostate cancer
What is the management of an AKI?
- Treat underlying cause: fluid rehydration, stop nephrotoxic medications, relieve obstruction
What are some complications of an AKI?
Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia - can lead to encephalopathy or pericarditis
What result on a urine albumin:creatinine ratio is significant?
> 3mg/mmol
What complications can you get in CKD?
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
What is first line to treat hypertension in patients with CKD?
ACE inhibitors - but serum potassium needs to be monitored!
What do you get in bloods in renal bone disease?
High serum phosphate (reduced phosphate excretion)
Low active vit D and so low calcium
Secondary hyperparathyroidism
What is osteosclerosis?
Osteoblasts respond by increasing their activity to match the osteoclasts but this new tissue is not properly mineralised due to the low calcium.
What causes acute interstitial nephritis?
Drugs (e.g. NSAIDs or antibiotics)
Infection
(hypersensitive reaction)
Often accompanied by rash, fever, eosinophilia
What are the main complications of hyperkalaemia?
Cardiac arrhythmias
Ventricular fibrillation
What can cause hyperkalaemia?
AKI
CKD
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
Aldosterone antagonists (spironolactone)
ACEi
ARBs
NSAIDs
Potassium supplements
What are the ECG changes in hyperkalaemia?
Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes
What is the management for hyperkalaemia?
Calcium gluconate - stabilises the cardiac muscle cells
Insulin and dextrose (act rapid 10 units and 50ml of 50% dextrose) - drives carbohydrates into cells and takes potassium with it
Also: nebulised salbutamol, IV fluids, calcium resonium, sodium bicarbonate, dialysis
What is acute tubular necrosis?
Necrosis of the epithelial cells of the renal tubules - usually due to AKI. These cells can regenerate so it is reversible after 7-21 days.
Caused by ischaemia or toxins (e.g. radiology contrast dye, gentamicin, NSAIDS)
What do you see on urinalysis in acute tubular necrosis?
Muddy brown casts
What is Type 1 Renal tubular acidosis?
The distal tubule is unable to excrete hydrogen ions
What can cause Type 1 Renal tubular acidosis?
Genetic
SLE
Sjogren’s syndrome
Primary biliary cirrhosis
Hyperthyroidism
Sickle cell anaemia
Marfan’s
How does Type 1 Tubular acidosis present?
Failure to thrive
hyperventilation
CKD
Bone disease
Hypokalaemia
Metabolic acidosis
High urinary pH
TREAT: oral bicarbonate
What is Type 2 Renal tubular acidosis?
Proximal tubule is unable to reabsorb bicarbonate
Usually caused by Fanconi’s syndrome
Same Ix and Mx as Type 1
What is Type 3 Renal tubular acidosis?
Mixture of type 1 and type 2
What is Type 4 Renal tubular acidosis?
Reduced aldosterone - most common cause
Due to adrenal insufficiency, ACEi, Spironolactone, SLE, Diabetes, HIV
What is different in the U&Es of Type 1 and 2, and Type 4?
Type 1 and 2 - hypokalaemia
Type 4. - Hyperkalaemia, high chloride, low urinary pH.
Both are metabolic acidosis
What is the management for Type 4 Renal Tubular Acidosis?
Fludrocortisone
Sodium bicarbonate and treatment of hyperkalaemia may be needed too
Is the autosomal dominant or autosomal recessive type of PKD more common?
Autosomal dominant
What are the autosomal dominant genes in PKD?
PKD-1: chromosome 16 (85%)
PKD-2: chromosome 4
What are the extra-renal manifestations of PKD?
Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian, prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation
What are the complications of PKD?
Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria
Renal stones
End-stage renal failure
How does autosomal recessive type PKD present?
Oligohydramnios in pregnancy (foetus doesn’t produce enough urine), leading to the underdevelopment of the lungs.
Rarer and more severe
What is the management of PKD?
Tolvaptan (a vasopressin receptor antagonist) - slows the development of cysts and progression of renal failure
What is the criteria for a Stage 2 AKI?
Creatinine rise x2 from baseline or
Reduced urine output of less than 0.5ml/kg/hr for 12 hours or more
What is the criteria for Stage 3 AKI?
Creatinine rise x3 from baseline within 7 days or
Creatinine rise to >354 micro mol/L with either acute rise (>26) in past 48 hrs or 50% rise from baseline in 7 days
Urine output of less than 0.3ml/kg/hr for 24 hrs
Anuria for 12 hrs
Any requirement for renal replacement therapy
What are the nephrotoxic drugs?
Aminoglycosides
Amphotericin
Cytotoxic drugs such as cisplatin
Diuretics
Immunosuppressants (E.g. ciclosporin and tacrolimus cause renal vasoconstriction
Radiocontrast
NSAIDs (renal hypo perfusion)
Lithium salts
How does the heart rate change from sitting to standing in hypovolaemia?
Rises by 30 or more
What is the equation for creatinine clearance?
(Urine creatinine x urine volume)/plasma creatinine
What % of cardiac output do kidneys get?
20%
What are the major endocrine functions of the kidney?
Secretion of EPO
Alpha1- hydroxylation of vit D
Production of Renin
What is creatinine
An ed product of skeletal muscle metabolism
When should creatinine clearance be used instead of plasma creatinine and GFR?
When the are highly significant falls of GFR (this can happen before serum creatinine rises)
What are the common causes of hypokalaemia
Diuretic therapy
Acute illness
GI losses
What are the features of hypokalaemia?
Weakness
Intestinal ileus
Decreased renal-concentrating ability
ECG changes: T-wave flattening, U waves, increased tachyarrhythmias
What are the three types of hyponatraemia?
Hypovolaemia
Normovolaemia
Hypervolaemia
What are common causes of hyponatraemia?
SIADH
Heart failure
Inappropriate IV dextrose in post op patients
Iatrogenic Addison’s disease (over-rapid corticosteroid withdrawal)
What are the signs of hypovolaemia?
Thirst
Tachycardia
Hypotension
Postural fall in BP
Reduced skin turgor
Why do you have to correct sodium carefully?
To avoid central pontine myelinolysis
What is central pontine myelinolysis?
Encephalopathy
Cranial nerve palsies
Quadriplegia
What are the most common causes of SIADH?
Idiopathic
Post op pain/infection/drugs
CNS: infection/stoke/neoplasia
Lung infection/tumour
Prostate/GI/haem malignancy
Drugs: Vasopressin, Carbemazepine, cyclophosphamide, aspirin
What are the features of nephritis?
haematuria, oliguria, proteinuria (moderate), fluid retention
What is the most common cause of nephritis?
IgA glomerulonephritis (Berger’s disease)
What age group does IgA glomerulonephritis particularly affect?
People in their 20s, often within 48hrs of an infection (e.g. URTI)
What is seen on histology in IgA glomerulonephritis?
IgA deposits
Mesangial proliferation
What is membranous nephropathy?
A type of glomerulonephritis where immune complexes deposit in the glomerular basement membrane, causing thickening and proteinuria (can also cause nephrotic syndrome)
What is seen on histology in membranous nephropathy?
IgG and complement deposits on the basement membrane
What are the causes of membranous nephropathy?
Idiopathic (70%)
Drugs such as: NSAIDs
Malignancy
SLE
What is membranoproliferative glomerulonephritis?
Immune complex deposits
Mesangial proliferation
Classically in people in under thirties
How soon after infection does post-streptococcal glomerulonephritis start?
Usually 1-6 weeks after streptococcal infection (e.g. tonsillitis or impetigo)
What is seen in histology in rapidly progressive glomerulonephritis?
Glomerular crescents
What is Goodpasture syndrome?
Anti-glomerular basement membrane syndrome
What antibodies are seen in Goodpasture syndrome?
Anti-glomerular basement membrane antibodies (a-GBM antibodies
What are the features of Goodpasture syndrome?
Haematuria
Pulmonary haemorrhage (antibodies also attack the basement membrane in the lungs): this can look like a ground glass appearance on CXR
What are the autoantibodies in microscopic polyangiitis?
p-ANCA
What are the autoantibodies in granulomatosis with polyangiitis?
c-ANCA
What investigation is used to find out the cause of the glomerulonephritis?
Renal biopsy is sometimes used - histology
