Renal Flashcards
When can an official diagnosis of an AKI be made ?
- Rise in serum creatinine of 26 micromol/litre or greater within 48 hours
- 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- Fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
What are the pre renal causes of an AKI ?
- Hypovolaemia secondary to D&V
- HF
- Renal artery stenosis
What are the intrinsic causes of AKI ?
- Glomerulonephritis
- Acute tubular necrosis (ATN)
- Acute interstitial nephritis (AIN)
- Rhabdomyolysis
- Tumour lysis syndrome
- HUS
What are the postrenal causes of AKI?
- Kidney stone in ureter or bladder
- BPH
- External compression of the ureter
what are the signs of an AKI?
- Reduced urine output
- Pulmonary and peripheral oedema
- Rise in K+ = arrhythmias
- Rise in urea / creatinine
- Features of uraemia (pericarditis / encephalopathy)
RF for an AKI
- CKD
- Other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
- History of AKI
- Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACEI/ARBs within the past week
- Use of iodinated contrast agents within the past week
- AGge >=65 years
What is acute tubular necrosis and what can it be caused by ?
- Most common cause of AKI
- Necrosis of renal tubular epithelial cells
- Caused by : ischaemia due to hypoperfusion or nephrotoxins
What will be seen on urinalysis in acute tubular necrosis ?
Muddy brown casts
What can cause acute interstitial nephritis ?
- Drugs : acute interstitial nephritis accounts for 25% of drug-induced AKI
- Systemic disease : SLE, sarcoidosis and Sjogrens
- Infection : Hanta virus, staphylococci
What drugs can cause acute interstitial nephritis
- Penicillin
- Rifampicin
- NSAIDs
- Allopurinol
- Furosemide
what will be seen on urinalysis in acute interstitial nephritis
- Sterile pyuria
- White cell casts
4 features of acute interstitial nephritis
- Fever, rash, arthralgia
- Eosinophilia
- Mild renal impairment
- HTN
what medications should be stopped in an AKI
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
what is involved in the management of AKI
- Careful fluid balance
- Stop any nephrotoxic medications
- Correction of hyperkalaemia if present
Give 5 causes of CKD
- Diabetes
- HTN
- Polycystic kidney disease
- Chronic glomerulonephritis
- Chronic pyelonephritis
what investigations are used to assess CKD
- eGFR
- Proteinuria quantified with urine albumin:creatinine ratio
- Haematuria
- Renal USS
How does nephrotic syndrome present ?
- Oedema
- Possible frothy urine due to the high protein content
How is CKD classified based on eGFR ?
- 1 : Greater than 90 ml/min, with some sign of kidney damage on other tests
- 2 : 60-90 ml/min with some sign of kidney damage
- 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
How is CKD classified based on albumin:creatinine ration ?
- A1 : <3mg/mmol
- A2 : 3-30 mg/mol
- A3 : >30mg/mol
what are the group of features seen in nephritic syndrome
-> Haematuria (blood in the urine), which can be microscopic (not visible) or macroscopic (visible)
-> Oliguria (significantly reduced urine output)
-> Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome)
-> Fluid retention
what is nephritis ?
Inflammation in the kidney
Primary causes of nephrotic syndrome
- Minimal change disease
- Focal segmental glomerulosclerosis (FSGS),
- Membranous nephropathy.
Most common type of inherited kidney disease
- AD
- PKD1 gene on chromosome 16 (85% of cases)
- PKD2 gene on chromosome 4 (15% of cases)
What is nephrotic syndrome ?
- The basement membrane of the glomerulus becomes highly permeable resulting in significant proteinuria
what are the group of features seen in nephrotic syndrome ?
- Proteinuria (more than 3g per 24 hours)
- Low serum albumin (less than 25g per litre)
- Peripheral oedema
- Hypercholesterolaemia
what is the eGFR based on ?
- Serum creatinine
- Age
- Gender
- Ethnicity
4 extra-renal manifestations of ADPKD
- Cerebral aneurysms
- Hepatic, splenic, pancreatic, ovarian and prostatic cysts
- Mitral regurgitation
- Colonic diverticula
6 complications of ADPKD
- Chronic loin/flank pain
- Hypertension
- Gross haematuria can occur with cyst rupture (usually resolves within a few days)
- Recurrent urinary tract infections
- Renal stones
- End-stage renal failure occurs at a mean age of 50 years
Presentation of ARKPD
- Picked up on antenatal scans with oligohydramnios
- Leads to pulmonary hypoplasia and resp failure shortly after birth
- Dysmorphic features (underdeveloped ear cartilage, low set eats, flat nasal bridge)
Chromosome involved in ARPKD
mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6
what can be given to slow the development of cysts and progression of renal failure in ADPKD
Tolvaptan (vasopressin receptor antagonist)
Causes of hyperkalaemia
D : Drugs (ACEI, ARB, NSAID, aldosterone antagonist)
R : Renal failure
E : Endocrine (Addison’s)
A : Artefact
D : DKA / DI
what 5 conditions can cause hyperkalaemia
Acute kidney injury
Chronic kidney disease (stage 4 or 5)
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
what ECG changes are seen in hyperkalaemia
Tall peaked T-waves
Flattening or absence of P waves
Prolonged PR interval
Broad QRS complexes
when do people require urgent treatment for hyperkalaemia
ECG changes
Serum potassium above 6.5 mmol/L
what is the treatment for hyperkalaemia
- Insulin and dextrose infusion and IV calcium gluconate
what is rhabdomyolysis and 5 possible causes
-> Skeletal muscle breakdown
- Prolonged immobility
- Extreme rigorous exercise
- Crush injuries
- Seizures
- Statins
What chemicals are released from muscle in rhabdomyolysis and why is this dangerous
Myoglobin = AKI
Potassium = arrythmias / arrest
Phosphate
Creatine kinase
7 signs and symptoms of rhabdomyolysis
Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)
Diagnostic blood test for rhabdomyolysis
-> Creatinine kinase (CK) : remains elevated for 1-3 days
what will a urine dipstick show in rhabdomyolysis
- Positive for blood due to presence of myoglobin (red-brown colour to urine)
Mainstay of treatment for rhabdomyolysis
- IV fluids to correct hypovolaemia and filter breakdown products
what is HUS and the usual trigger ?
- Thrombosis in small blood vessels
- Triggered y shiga toxins for E.coli O157 or Shigella
Who does HUS usually affect and what increases the risk of it ?
- Children following an episode of gastroenteritis
- Abx and anti-motility medication (e.g. loiperamide)
what triad is seen in HUS ?
- AKI
- Thromboytopenia (formation of blood clots)
- Microangiopathic haemolytic anaemia
what is the presentation of HUS ?
- Diarrhoea from gastroenteritis, turns blood in 3 days
- After a week, Sx of HUS develop :
Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion
How is HUS managed
-> Medical emergency = admit and treat :
Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)
Correction of hypokalaemia due to diarrhoea
IV sodium chloride with IV potassium chloride at 10mmol/hour
Secondary causes of nephrotic syndrome
- DM
- SLE
- Amyloidosis
- Infections (HIV, hepatitis B and C), - Drugs (NSAIDs, gold therapy).
Common presentation of amyloidosis
- 50-65 yr old
- Worsening SOB and weakness
- Loss of renal function & proteinuria
- Massive hepatosplenomegaly
Results in keeping with a diagnosis of acute tubular necrosis
- Raised urinary sodium
What urea to creatinine ratio would suggest a pre renal cause of an AKI
Urea rise»_space;» Creatinine rise
- Urea : creatinine ratio of >100
- In pre renal causes, blood flow to kidney is reduce and so kidneys reabsorb more water and solutes including urea
New onset chest pain on a background of CKD with raised urea
Pericarditis caused by uraemia
Treatment of encephalopathy (confusion) or pericarditis caused by uraemia
Haemodialysis
- Presents with allergic type reaction after commencing new medication
- Fever, joint pains
- Pruritic macular rash
- AKI
Diagnosis and what will be seen on urinalysis
Acute interstitial nephritis
White cell casts
How do u calculate an anion gap
(Sodium + potassium) - (bicarbonate + chloride)
How is the anion gap used to classify metabolic acidosis
- Raised anion gap = DKA
- Normal = seen in pts with diarrhoea due to GI bicarb loss
Management of anaemia due to CKD
Oral iron (if not on ESAs or haemodialysis)
IF target Hb Levels in a pt with anaemia caused by CKD are not reached within 3 mnths of oral iron what should they be switched too ?
IV iron
If a patient on ESAs or haemodialysis develop anaemia due to CKD what do they generally require
IV iron
Screening test for adult ADPKD
Abdominal USS
USS diagnostic criteria for ADPKD (In pts with a +ve family history)
- Two cysts, unilateral or bilateral, if aged < 30 years
- Two cysts in both kidneys if aged 30-59 years
- Four cysts in both kidneys if aged > 60 years
What are pts with ADPKD at risk of ?
Subarachnoid haemorrhage due to ruptured berry aneurysms
what cardiac condition is ADPKD associated with
Mitral valve prolapse
Most common cause of post operative oliguria
Hypovolaemia
Management of poster operative oliguria if stab le and not clinically fluid overload
Fluid challenge = 500ml fluid bolus
What can be seen on microscopic examination of urine in acute interstitial nephritis ?
Eosinophilic casts
Investigation of AKI of unknown origin
Renal USS
What is the exception to the rule of stopping NSAIDs in AKI
Aspirin at cardio-protective doses
Stage 1 AKI
- Increase in creatinine to 1.5-1.9 times baseline, or
- Increase in creatinine by ≥26.5 µmol/L, or
- Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage 2 AKI
- Increase in creatinine to 2.0 to 2.9 times baseline, or
- Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
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
What is the primary action of ADH
- Acts on the kidney to increase the reabsorption of water
Cranial DI
Decreased secretion of ADH from the pituitary
Causes of cranial DI
- Idiopathic
- Post head injury
- Pituitary surgery
- Craniopharyngiomas
- Infiltrative : histiocytosis X, sarcoidosis
- DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
- Haemochromatosis
Nephrogenic DI
Insensitivity of the kidney to ADH
Causes of nephrogenic DI
- Genetic:
- Electrolytes : hypercalcaemia, hypokalaemia
- Lithium
- Demeclocycline
- Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
Features of DI
Nocturia
Polyuria
Polydipsia
Gold standard investigation for DI
Water deprivation test
Investigation findings in DI
high plasma osmolality
low urine osmolality
Management of nephrogenic DI
thiazides
low salt/protein diet
Management of cranial DI
Desmopressin - vasopression V2 agonist
Management of ascites in pts with chronic liver disease
- Aldosterone antagonist = spironolactone
Type of tubulointerstitial nephritis seen in young females
Tubulointerstitial nephritis with uveitis
Fever, weight loss, painful red eyes
Leukocytes and protein on urinalysis
why does urinary sodium decrease in pre renal causes of AKI
- The kidneys reabsorb more sodium in order to preserve volume
U&E result suggest kidney disease is chronic and not acute
Hypocalcaemia
First line management of pts with proteinuria that have CKD and coexistent HTN if the ACR >30mg/mmol
ACEI
If max dose ACEI is not efficient in managing proteinuia in pts with CKD + ACR >30 what can be added
SGLT-2 inhibitor
Direct complication of nephrotic syndrome
Increased VTE risk -> prophylactic LMWH required
Cause of ABG showing metabolic acidosis (low HCO3, normal CO2) with a NORMAL anion gap and possible hypokalaemia
Diarrhoea
what does vomiting show on an ABG
- Metabolic alkalosis = loss of gastric secretions which are acidotic
- Hypochloraemia, hypokalaemia
Most common cause of nephrotic syndrome in adults and often associated with malignancy
Membranous nephropathy
Renal biopsy in membranous nephropahty
- Thickened basement membrane
- Subepithelial electron dense deposist
Management of membranous nephropathy
- ACEI to reduce proteinuria
Cause of metabolic acidosis with raised chloride
Large volume fluid resuscitation with 0.9% sodium chloride
what would suggest the cause of AKI is intrinsic ?
- Urea : creatinine ration of <100
- No response to fluid challenge
Common cause of nephrotic syndrome in pts with HIV
Focal segmental glomerulosclerosis
Common presenting history causing tubular cell necrosis
- Fall with prolonged lie
- Rhabdomyolysis = myoglobinuria
- Causes acute tubular cell necrosis
what are pts who have had an organ transplant and are on long term immunosuppression at increased risk of ?
- Skin cancer -> esp squamous cell carcinoma
Signs of an under-filled fluid balance
- Tachycardia
- Hypotension
- Oliguria
- Sunken eyes and reduced skin turgor
Pt presents >24hrs after paracetamol overdose + jaundice, hepatic tenderness or elevated ALT
Start acetylcysteine
Pt presents 8-24 hrs after paracetamol overdose of more than 150mg/kg
Start acetycysteine
When should acetylcysteine be given for paracetamol overdose
- Plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
- Staggered overdose or doubt over time of ingestion
Presentation of renal adenocarcinoma
- HTN and haematuria
- Associated polycythamie a
- Left renal mass
Presentation of transitional cell carcinoma
- Ureteric colic
- Heematuria
- Dilatation of renal pelvis but outline is irregular
Presentation of nephroblastoma
- 4 y/o
- Haematuria
- Renal mass
It is also known as Wilms tumours
small vessel vasculitis causing pullmonary haemorrhage and glomerulonephritis
Granulomatosis with polyangitis = Anti-glomerular basement membrane disease (Goodpastures)
Presentation of anti-glomerular basement membrane disease
- Haemoptysis and SOB
- Proteinuria and haematuria
Antibodies seen in granulomatosis with polyangitis
ANCA
Anti-glomerular basement membrane
Most common cause of glomerulonephritis world wide
IgA nephropathy
Features of IgA nephropathy
- Preceeding URTI
- 3 days later -> frank haematuria, no or little protein.
what is seen histologically in IgA nephropathy
- Mesangial hypercellularity
- Positibe immunofluoresecene for IgA and C3
Treatment of IgA nephropathy if persistnent proteinuria
ACEI
Presentation of Wilms’ nephroblastoma
- Child <5
- Painless haematuria
- Abdominal mass
Most common cause of peritonitis associated with peritoneal dialysis
Staphylococcus epidermis
4 common causes of polyuria
- Lithium
- HF
- DM
- Diuretics, caffeine and alcohol
what is seen on the bloods in post streptococcal glomerulonephritis
- Low C3
- Raised anti-streptolysin O titre confirms a recent strep infection
How to reduce the risk of contrast induced nephropathy
IV 0.9% sodium chloride pre and post procedure
Presentation of alport’s syndrome in a child
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural hearing loss
5 causes of metabolic acidosis with a normal anion gap (Hyperchloraemic metabolic acidosis)
- GI bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
- Renal tubular acidosis
- Drugs: e.g. acetazolamide
- Ammonium chloride injection
- Addison’s disease
4 causes of metabolic acidosis with a raised anion gap
- Lactate: shock, hypoxia
- Ketones: diabetic ketoacidosis, alcohol
- Urate: renal failure
- Acid poisoning: salicylates, methanol
8 causes of metabolic alkalosis
Caused by either loss of H+ or gain of bicarbonate
- Vomiting
- Diuretics
- Hypokalaemia
- Primary hyperaldosteronism
- Cushing’s syndrome
- Bartter’s syndrome
- Congenital adrenal hyperplasia
- Liquorice, carbenoxolone
3 causes of respiratory acidosis
- COPD
- Decompensatation of resp conditions : Asthma, pulmonary oedema
- Sedative drugs : Opiate overdose, benzos
6 causes of respiratory alkalosis
- PE
- Anxiety : Hyperventilation
- CNS disorders : stroke, SAH, encephalitis
- Altitude
- Pregnancy
- Salicylate poisoning
how should diabetics be screened for diabetic nephropathy
annually using albumin:creatinine ratio (ACR)
When should an ACEI be started for diabetic nephropathy
If urinary ACR is 3mg/mmol or more
Management of diabetic nephropathy
- Dietary protein restriction
- Tight glycaemic control
- BP control: aim for < 130/80 mmHg
- ACEI
- Control dyslipidaemia e.g. Statins
4 presenting features of henoch-schonlein purpura
- Palpable purpuric rash over buttock and extensor surface
- Abdo pain
- Polyarthritis
- IgA nephropathy : haematuria, renal falure
what should parents be educated on monitoring in HSP
BP and urinalysis for progressive renal involvmenet
5 complications of nephrotic syndrome
- Increased risk of VTE
- Hyperlipidaemia
- CKD
- Increased risk of infection
- Hypocalcaemia
Presentation of post-streptococcal glomerulonephritis
Strep pyogenes infection 7-14 days prior
- Visible haematuria
- Headache, malaise
- HTN
- Oliguria
5 causes of rhabdomyolysis
- Seizure
- Collapse/coma (e.g. elderly patient collapses at home, found 8 hours later)
- Ecstasy
- Crush injury
- Drugs: statins (especially if co-prescribed with clarithromycin)
Risk in creatining kinase required for diagnosis of rhabdomyolysis
5 times upper limit of normal
