Nephrology Flashcards
Drugs causing acute interstitial nephritis
Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide
Systemic disease causing acute interstitial nephritis
SLE
Sarcoidosis
Sjorgen’s syndrome
Infections causing acute interstitial nephritis
Hanta virus
Staphylococci
Features acute interstitial nephritis
Fever
Rash
Arthralgia
Hypertension
Blood tests acute interstitial nephritis
Eosinophilia
Mild renal impairmentU
Urine acute interstitial nephritis
Sterile pyuria
White cell casts
Demographic tubulointerstitial nephritis with uveitis
Young females
Symptoms tubulointerstitial nephritis with uveitis
Fever
Weight loss
Painful, red eyes
Urinalysis tubulointerstital nephritis with uveitis
Positive with leukocytes and protein
Best way to differentiate AKI and CKD
Ultrasound - CKD have bilaterally small kidneys
Causes of CKD without bilaterally small kidneys
- Autosomal dominant polycytic kidney disease
- Diabetic nephropathy
- Amyloidosis
- HIV assocaited nephropathy
Blood tests suggesting CKD rather than AKI
Hypocalcaemia
AKI criteria
Rise in serum creatinine of 26 micromol/L or greater in 48 hours
50% or greater rise in creatinine known or presumed to have happened within past 7 days
Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours
Investigation AKI
If no cause or risk of urinary tract obstruction, renal ultrasound within 24 hours of assessment
Drugs that should be stopped in AKI as may worsen renal function
NSAIDs
Aminoglycosides
ACE inhibitors
ARBs
Diuretics
Drugs that should be stopped in AKI due to toxicity
Metformin
Lithium
Digoxin
Indications for RRT in AKI
- Not responding to medical treatment
- Complications
Complications of AKI
Hyperkalaemia
Pulmonary oedema
Acidosis
Uraemia (pericarditis, encephalitis)
How to differentiate between pre-renal uraemia and acute tubular necrosis?
- In pre-renal uraemia, urine sodium <20mmol/L and urine osmolality >500. In ATN, urine sodium >40 and urine osmolality <350
- In pre-renal uraemia, good response to fluid challenge. In ATN, poor response
- In pre-renal uraemia, serum urea:creatinine ratio raised. In ATN, normalN
Stage 1 AKI
Increase in creatinine 1.5-1.9x baseline, or
Increase in creatinine ≥26.5, or
Reduction in urine output to <0.5ml/kg/hour for ≥6 hours
Stage 2 AKI
Increase in creatinine to 2.0 - 2.9x baseline, or
Reduction in urine output <0.5ml/kg/hour for ≥12 hours
Stage 3 AKI
Increase in creatinine ≥3.0 times baseline, or
Increase in creatinine to ≥353.6, or
Reduction in UO to <0.3ml/kg/hour for ≥24 hours. or
Initiation of RRT, or
In patients <18, decrease in eGFR to <35
Criteria for referral to nephrologist AKI
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 RRT
ADPKD type 1 vs 2
ADPKD 1 more common, presents with renal failure earlier
Screening modality ADPKD
Ultrasound
Ultrasound diagnostic criteria ADPKD
- 2 cysts, unilateral or bilateral if aged <30
- 2 cysts in both kidneys if aged 30-59
- 4 cysts in both kidneys if >60
Management ADPKD
Tolvaptan (in select patients)
Purpose of tolvaptan in ADPKD
Slow progression of cyst development and renal insufficiency
Criteria for tolvaptan use ADPKD
CKD stage 2 or 3
Evidence of rapidly progressive disease
Company provides it with discount agreed in patient access scheme
Features ADPKD
Hypertension
Recurrent UTIs
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones
Extra-renal manifestations ADPKD
Liver cysts
Berry aneurysms
Cardiovascular system
Cysts in other organs
ADPKD cardiovascular system
Mitral valve prolapse
Mitral/tricuspid incompetence
Aortic root dilatation
Aortic dissection
What other organs get cysts in ADPKD
Liver (70%)
Pancreas
Spleen
Rarely:
Thyroid
Oesophagus
Ovary
Inheritance pattern Alport syndrome
X-linked dominant
When does Alports syndrome present
Childhood
Features Alports syndrome
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus
Retinitis pigmentosa
What is lenticonus
Protrusion of the lens surface into the anterior chamber
Investigations Alport syndrome
Molecular genetic testing
Renal biopsy
Renal biopsy findings Alport syndrome
Longitudinal splitting of lamina densa of GBM, resulting in basket weave appearance
Boys vs girls Alport syndrome
Disease more severe in males, females rarely develop renal failure
Cause of failing renal transplant in Alport’s syndrome
Presence of anti-GBM antibodies, leading to Goodpastures syndrome like picture
How to calculate anion gap
(Sodium + potassium) - (bicarb + chloride)
Normal anion gap
8-14
Causes of normal anion gap or hyperchloraemic metabolic acidosis
GI bicarb loss - diarrhoea, uterosigmoidostomy, fistula
Renal tubular acidosis
Drugs, e.g. acetazolamide
Ammonium chloride injection
Addison’s disease
Causes of raised anion gap metabolic acidosis
Lactate - shock, hypoxia
Ketones - diabetic ketoacidosis, alcohol
Urate - renal failure
Acid poisoning - salicylates, methanol
5-oxoprolone - chronic paracetamol use
Causes of anaemia in renal failure
- Reduced erythropoietin levels
- Reduced absorption of iron
- Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
- Anorexia/nausea due to uraemia
- Reduced red cell survival
- Blood loss due to capillary fragility and poor platelet function
- Stress ulceration leading to chronic blood loss
Targe haemoglobin in CKD
10-12
Treatment anaemia in CKD
Iron administration (prior to starting…)
Erythropoiesis-stimulating agents
Route of administration of iron
Iron if not on ESAs or dialysis. If target Hb not reached in 3 months, switch to IV
If on ESAs or dialysis, IV iron
Examples erythropoiesis stimulating agents
Erythropoietin
Darbepoetin
GFR anaemia is seen at in CKD
Usually <35 (consider alternative diagnosis if >60
Type of anaemia seen in CKD
Normochromic normocytic
Complication anaemia in CKD
Left ventricular hypertrophy
Common causes CKD
Diabetic nephropathy
Chronic glomerulonephritis
Chronic pyelonephritis
Hypertension
Adult PKD
CKD dietary advice
Low protein
Low phosphate
Low sodium
Low potassium
What factors make up GFR
Serum creatinine
Age
Gender
Ethnicity
Factors that might affect GFR result
Pregnancy
Muscle mass, e.g. amputees, body builders
Eating red meat 12 hours prior to sample being taken
Stage 1 CKD GFR
Greater than 90, with some signs of kidney damage on other testS
Stage 2 CKD
60-90, with some sign of kidney damage
Stage 3a CKD
45-59
Stage 3b CKD
30-44
Stage 4 CKD
15-29
Stage 5 CKD
Less than 15
First line anti-hypertensive CKD
ACE inhibitors
What level of derangement in U&E is acceptable when starting ACEi in CKD
Decrease in GFR 25%
Rise in creatinine up to 30%
What to consider if greater derangement in U&E after starting ACEi in CKD
Renovascular disease
Role of furosemide CKD
Useful as anti-hypertensive, particularly when GFR below 45
Added benefit of lowering potassium
Causes of cranial DI
Idiopathic
Post head injury
Pituitary surgery
Craniopharyngiomas
Infiltrate - histiocytosis X, sarcoidosis
Wolframs syndrome
Haemochromatosis
What is Wolframs syndrome
Association of;
- Cranial DI
- Diabetes mellitus
- Optic atrophy
- Deafness
Causes nephrogenic DI
Genetic
Hypercalcaemia
Hypokalaemia
Lithium
Demeclocycline
Tubulo-interstitial disease - obstruction, sickle cell, pyelonephritis
Investigation DI
High plasma osmolality, low urine osmolality
Water deprivation test
What urine osmo excludes diabetes insipidus
> 700
Management nephrogenic diabetes insipidus
Thiazides
Low salt/protein diet
Management central diabetes insipidus
Desmopressin
Maintenance fluid requirements
25-30ml/kg/day water
1mmol/kg/day potassium, sodium, chloride
50-100g/day glucose
Risk of large volumes of 0.9% saline
Hyperchloraemic metabolic acidosis
Causes of transient or spurious non-visible haematuria
UTI
Mensturation
Vigorous exercise
Sexual intercourseC
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
Causes of red/orange urine with neg blood dipstick
Foods - beetroot, rhubarb
Drugs - rifampicin, doxorubicin
What is defined as persistent non-visible haematuria
Blood being present in 2 out of 3 samples tested 2-3 weeks apart
Further investigations haematuria
Bloods - renal function, albumin:creatinine ratio or protein:creatinine ratio, BP
Limitation urine microscopy in haematuria
Time to analysis significantly affects number of RBC detectedU
Criteria 2WW with haematuria
Age ≥45 with:
- Unexplained visible haematuria without UTI
- Visible haematuria that persists or recurs after successful treatment of UTI
Age ≥60 and unexplained non-visible haematuria and either dysuria or raised WCC on bloods
Criteria non-urgent referral for haematuria
Age ≥60 with recurrent or persistent unexplained urinary tract infection
Triad seen in HUS
AKI
Microangiopathic haemolytic anaemia
Thrombocytopenia
Causes HUS
Most cases secondary:
Shiga toxin-producing E coli 0157:H7 (90% of cases in children)
Pneumococcal infection
HIV
SLE
Drugs
Cancer
Primary HUS due to complement dysregulation
Investigation in HUS
Blood film (most useful test)
U&E
Stool culture
Blood film finding in HUS
Intravascular red blood cell fragmentation → formation of schistocytes
Hb <80
Thrombocytopenia
U&E in HUS
AKI
Stool culture in HUS
May show evidence of STEC infection
Management HUS
Supportive treatment - fluids, blood transfusion, dialysis
Indications for plasma exchange in HUS
Complicated - in general, reserved for severe cases of HUS not associated with diarrhoea
Medicine used in treatment of HUS
Eculizumab - greater efficacy than plasma exchange alone in treatment of adult atypical HUS
What is HSP
IgA mediated small vessel vasculitis
Features HUS
Palpable purpuric rash with localised oedema over buttocks and extensor surfaces of arms and legs
Abdominal pain
Polyarthritis
Features of IgA nephropathy may occur - haematuria, renal failure
Treatment HUS
Supportive
Prognosis HUS
Usually excellent - self-limiting condition, esp in children without renal involvement
Monitoring HUS
BP and urinalysis to detect renal involvement
ECG changes hyperkalaemia
Tall tented T waves
Loss of P waves
Broad QRS
Sinusoidal wave pattern
Treatment to stabilise myocardium in hyperkalaemia
IV calcium gluconate
Treatment to short-term shift potassium ECF → ICF in hyperkalaemia
Insulin/dex
Salbutamol nebs
Treatment to remove potassium from body
Calcium resonium (orally or enema)
Loop diuretics
Dialysis
Features hypokalaemia
Muscle weakness
Hypotonia
ECG hypokalaemia
U waves
Small or absent T waves
Prolonged PR interval
ST depression
Conditions associated with IgA nephropathy
Alcoholic cirrhosis
Coeliac disease/dermatitis herpetiformis
HSP
IgA nephropathy also known as
Berger’s disease
Classic presentation IgA nephropathy
Macroscopic haematuria in young people following URTI
Histology IgA nephropathy
Mesangial hypercellularity, positive immunoflourescence for IgA and C3
IgA nephropathy vs post-streptococcal glomerulonephritis
Post streptococcal glomerulonephritis associated with low complement levels
Main symptom in post-streptococcal glomerulonephritis is proteinuria
Typically interval between URTI and onset of renal problems in post-streptococcal glomerulonephritis
When is no treatment needed IgA nephropathy
Isolated haematuria, no or minimal haematuria (less than 1000mg/day), and normal GFR
Just f/u to check renal function
Treatment IgA nephropathy when persistent proteinuria but normal/slightly reduced GFR
ACE inhibitors
Treatment IgA nephropathy if active disease (falling GFR) or failure to respond to ACEi
Immunosuppression with corticosteroids
Prognosis IgA nephropathy
25% develop ESRF
Markers of good prognosis IgA nephropathy
Frank haematuria
Markers of poor prognosis IgA nephropathy
Male gender
Proteinuria, esp >2g/day
Smoking
Hypertension
Hyperlipidaemia
ACE genotype DD
Cause normal anion gap metabolic acidosis
- GI bicarb loss (diarrhoea, ureterosigmoidoscopy, fistula)
- Renal tubular acidosis
- Drugs, e.g. acetazolamide
- Ammonium chloride injection
- Addison’s disease
Causes raised anion gap metabolic acidosis
- Lactate - shock, sepsis, hypoxia
- Ketones - diabetic ketoacidosis
- Urate - renal failure
- Acid poisioning - salicylates, methanol
Division of metabolic acidosis secondary to high lactate
Type A - sepsis, shock, hypoxia, burns
Type B - metformin
Causes minimal change disease
Majority of cases idiopathic
In 10-20% cases, cause found:
- Drugs
- Hodgkin’s lymphoma
- Thymoma
- Infectious mononucleosis
Drugs causing minimal change disease
NSAIDs
Rifampicin
Features minimal change disease
Nephrotic syndrome
Normotension
Highly selective proteinuria
Features of proteinuria in minimal change disease
Only intermediate sized proteins such as albumin and transferrin leak through the glomerulus
Renal biopsy in minimal change disease
Normal glomeruli on light microscopy
Electron microscopy shows fusion of podocytes and effacement of foot processes
First line treatment minimal change disease
Oral corticosteroids
80% steroid responsive
Second line treatment minimal change disease
Cyclophosphamide
Definition contrast media nephrotoxicity
25% increase in creatinine occurring within 3 days of intravascular administration of contrast media
Management of metformin around contrast procedures
Hold 48 hours before and until renal function normal - reduce risk of lactic acidosis
Complications peritoneal dialysis
Peritonitis
Sclerosing peritonitis
Most common cause of peritonitis in peritoneal dialysis
Coagulase neg staph e.g. Staphylococcis epidermidis
Antibiotics peritonitis caused by peritoneal dialysis
Vanc (or teic) + ceftazidime added to dialysis fluid
or
Vancomycin added to dialysis fluid and ciprofloxacin by mouth
Bacteria causing post-streptococcal glomerulonephritis
Group A beta haemolytic streptococcus, usually streptococcus pyogenes
Timeline post-streptococcal glomerulonephritis
Typically 7-14 days after infection
Pathophysiology post-streptococcal glomerulonephritis
Immune complex (IgG, IgM, C3) deposition in glomeruli
Features post-streptococcal glomerulonephritis
- Headache
- Malaise
- Proteinuria, may result in oedema
- Hypertension
- Oliguria
Bloods post-streptococcal glomerulonephritis
Raised anti-streptolysin O titre (confirm recent streptococcal infection)
Low C3
Renal biopsy in post-streptococcal glomerulonephritis
Acute, diffuse proliferative glomerulonephritis
Endothelial proliferation with neutrophils
Subepithelial humps caused by lumpy immune deposits on electron microscopy
Granular or starry sky appearance on immunoflourescence
Post-op renal transplant problems
ATN graft
Vascular thrombosis
Urine leakage
UTI
When does hyperacute rejection of renal transplant occur
Minutes to hours
Cause hyperacute rejection renal transplant
Pre-existing antibodies against ABO or HLA antigens
What kind of hypersensitivity reaction hyperacute rejection renal transplant
Type II hypersensitivity reaction
Pathophysiology hyperacute rejection renal transplant
Widespread thrombosis of graft vessels → ischaemia and necrosis of transplanted organ
Management hyperacute rejection renal transplant
No treatment possible, graft must be removed
Timeline acute graft failure renal transplant
<6 months
Cause acute graft failure renal transplant
Usually mismatched HLA causing cell-mediated (cytotoxic T cells) reaction
Other causes include CMV infection
Presentation acute graft failure renal transplant
Usually asymptomatic, picked up with rising creatinine, pyuria, proteinuria
Treatment acute graft failure renal transplant
May be reversible with steroids and immunosuppressants
Timeline chronic graft failure
> 6 months
Causes chronic graft failure
- Chronic allograft nephropathy
- Recurrence of original renal disease
What happens in chronic graft nephropathy
Both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney
Initial immunosuppression renal transplant
Ciclosporin/tacrolimus with monoclonal antibody
Maintenance immunosuppression renal transplant
Ciclosporin/tacrolimus with mycophenolate mofetil or sirolimus
When should steroids be added renal transplant immunosuppression
If more than one steroid responsive acute rejection episdoe
Advantages tacrolimus over ciclosporin
Lower incidence of acute rejection
Less hypertension and hyperlipidaemiai
Disadvantages tacrolimus over ciclosporin
High incidence of impaired glucose tolerance and diabetes
SEs mycophenolate mofetil
GI and marrow suppression
SEs sirolimus
Hyperlipidaemia
Complications long term immunosuppression
Cardiovascular disease
Renal failure
Malignancy
Malignancy advice for patients on immunosuppressants after renal transplant
Education about minimising sun exposure to reduce risk of squamous cell carcinoma and basal cell carcinoma
Causes rhabdomyolysis
Seizure
Collapse/coma
Ecstasy
Crush injury
McArdle’s syndrome
Drugs
Drugs causing rhabdo
Statin, esp if co-prescribed with clarithromycin
Features rhabdomyolysis
AKI with disproportionately raised creatinine
Elevated CK (at least 5x upper limit of normal)
Myogloburia
Hypocalcaemia
Elevated phosphate
Hyperkalaemia
Metabolic acidosis
Management rhabdomyolysis
IV fluids to maintain good urine output
Urinary alkalinisation sometimes used
Indications spironolactone
Ascites
Hypertension
Heart failure
Nephrotic syndrome
Conn’s syndrome
Adverse effects spironolactone
Hyperkalaemia
Gynaecomastia
