Renal Flashcards
Causes of pre-renal AKI
Low BP
Low cardiac output
Renal artery stenosis
Decreased intravascular volume
Causes of intrinsic AKI
Acute tubular necrosis (can be causes by rhabdomyolysis) Nephrotoxic drugs Contrast dye Interstitial nephritis Glomerulonephritis Vasculitis
Causes of post-renal AKI
BPH
Bladder cancer
Calculi
Obstruction
Which medication classes are nephrotoxic
NSAIDs ACEi ARBs Gentamycin Contrast dye
Stage 1 AKI
Serum creatinine >26 or 1.5-2x baseline
Urine output <0.5ml/kg/hr for >6 hours
Stage 2 AKI
Serum creatinine 2-3x baseline
Urine output <0.5 ml/kg/hr for >12 hours
Stage 3 AKI
Serum creatinine >354 or >3x baseline or on RRT
Urine output <0.3 ml/kg/hr for >24 hours or anuric for >12 hours
Complications of AKI
High K
Pulmonary oedema/fluid overload if low urine output
Metabolic acidosis (kidney usually excretes H+)
Uraemic encaphalopathy
Uraemic pericarditis
Low Ca, high PO4
ECG changes in hyperkalaemia
Small or no P waves Prolonged PR interval Wide QRS Peaked T waves Slurring into ST VF
Treatment of hyperkalaemia
IV Calcium gluconate or calcium chloride to stabilise the cardiac membranes Beta-agonists to move K into cells Bicarbonate to move K into cells IV insulin to move K into cells IV NaCl to increase renal K excretion Diuretics to increase renal K excretion Haemodialysis
Phases of AKI
Symptoms of underlying illness
Oliguric/anuric phase - low UO, high urea and creatinine, fluid retention, pulmonary oedema, hyperkalaemia, metabolic acidosis, lethargy, asterixis, uraemic encephalopathy/pericarditis. Lasts less than 2 weeks.
Polyuric/maintenance phase - filtration resumes but reabsorption still impaired, polyuria, low Na, low K. Lasts around 3 weeks
Recovery phase - renal function and urine production return to normal, can take up to 2 years
BUN:Creatinine ratio in pre-renal Vs intrinsic AKI
BUN:Cr basically tells you whether or not the tubules are still functioning
Creatinine is produced at a constant rate and all of it is excreted, non is reabsorbed, whereas urea is partially reabsorbed and affected by diet ect
In pre-renal AKI as normal all Cr is excreted, tubules are still working and reabsorbing urea so serum urea is higher. So BUN:Cr >20:1
In intrinsic AKI as normal all Cr is excreted, tubules aren’t working though so more urea being excreted than normal so less serum urea compared to pre-reanl. So BUN:Cr <20:1 (closer to 1)
Describe the urine Na concentration and urine osmolality in pre-renal AKI
Decreased renal blood flow but tubules still working
RAAS activated causing Na and H2O retention
Concentrated urine - high osmolality >500 but looking at just urine Na concentration this is low <20 because Na is being reabsorbed by the still-functioning tubules
Describe the urine Na concentration and urine osmolality in instrinsic AKI
Tubules damaged so cant function and cant reabsorb Na. So Na and H2O lost in urine - dilute urine with a high Na concentration. Low urine osmolality <350, high urinary Na concentration >40
What does low BP do to the afferent and efferent arterioles
Dilates the afferent, constricts the efferent
What does high BP do to the afferent and efferent arterioles
Constricts the afferent, dilates the efferent
Why are ACE inhibitors and NSAIDs nephrotoxic?
They interfere with compensatory mechanisms that maintain eGFR;
ACEi dilate the efferent arteriole
NSAIDs block prostaglandins that normally dilate the afferent arteriole (effectively constricting the afferent arteriole)
How do CKD affected kidneys appear on USS
Small with increased echogenicity
Why do you get polyuria/oedema/anaemia in CKD
Polyuria due to inability to concentrate urine (can’t reabsorb water, decreases urine osmolality)
Oedema due to proteinuria (can’t reabsorb protein) which decreases intravascular osmotic pressure so fluid leaks out of vessels
Normochromic normocytic anaemia due to decreased EPO production
Why do you get low Ca and high PO4 in CKD
Decreased renal function causes decreased activation of VitD so decreased production of calcitriol so decreased intestinal absorption of calcium
Decreased renal function results in less excretion of PO4
Stages of CKD (GFR)
1 - >90 but with persistent albuminuria or hereditary renal disease 2 - 60-89 3a - 45-59 3b - 30-44 4 - 15-29 5 - <15 (end stage renal failure)
What are the 3 main things that can cause acute tubular necrosis? (ATN)
Prolonged/severe renal ischaemia
Nephrotoxins
Myoglobinuria/haemoglobinuria
What is the normal rate of urination for a healthy person?
0.5ml/kg/hr
Causes of CKD
Hypertension
Diabetes
Renal artery stenosis
Congenital/inherited - PCKD, Alports syndrome, medullary cystic disease
Glomerular disease - IgA nephropathy, Wegeners granulomatosis, amyloidosis, sickle cell
Interstitial disease - reflux nephropathy, TB, multiple myeloma
What are the signs and symptoms of CKD
Malaise, loss of appetite, insomnia, restless leg syndrome, nocturia, polyuria (inability to concentrate urine), itching, nausea, vomiting, diarrhoea, peripheral and pulmonary oedema, bruising, bone pain due to metabolic bone disease, anaemia (pallor)
What type of anaemia does CKD cause?
Normochromic, normocytic
Features of nephrotic syndrome and why they happen
- Proteinuria (due to loss of podocytes), >3g/24hrs or P:Cr >300, A:Cr >250
- Oedema (hypoalbuminuria due to urinary protein loss lowers intravascular oncotic pressure)
- Hypoalbuminaemia (<30g/L)
Hyperlipidaemia (hypoalbuminaemia causes liver to increase protein production to compensation and this causes lipid production to also increase)
Hypercoagulable state due to urinary loss of antithrombin 3
Features of nephritic syndrome
Haematuria Hypertension (due to low GFR causing fluid retention) Oliguria (due to low GFR) Azotaemia due to decreased excretion RBC casts Proteinuria
Difference in pathophysiology between nephrotic syndrome and nephritic syndrome
Nephrotic due to loss of podocytes so features are due to the resulting proteinuria
Nephritis due to immune complex deposition and inflammation in the glomeruli which damages the glomerulus and lowers GFR - resulting features are due to the low GFR
Causes of nephritic syndrome
IgA nephropathy HSP Post-strep glomerulonephritis Goodpasteurs syndrome Rapidly progressive GN (small vessel/ANCA vasculitis, SLE)
Causes of nephrotic syndrome
Minimal change disease Focal segmental glomerulosclerosis Membranous nephropathy Membranoproliferative glomerulonephritis DM SLE Myeloma Amyloidosis
Two main causes of acute nephritic syndrome
Post-strep glomerulonephritis
IgA nephropathy
Management of nephrotic syndrome
Salt restriction Fluid restriction (1-1.5L/24hrs) Loop diuretics Add ACEi/ARBs reduce proteinuria VTE prophylaxis Renal biopsy
What are the 3 types of rapidly progressive/crescenteric glomerulonephritis
Type 1 (Goodpasteurs) - linear immunofluorescence Type 2 (immune complex mediated) - granular immunofluorescence Type 3 (pauci-immune/vasculitic) - negative immunofluorescence
Which diseases are included in Type 2 RPGN
Post-strep GN
SLE
IgA nephropathy
HUS
Which diseases are included in Type 3 RPGN
Granulomatosis with polyangitis (Wegeners)
Microscopic polyangitis
Eosinophilic granulomatosis with polyangitis (Churg-Strauss)
cANCA positive vasculitis
GPA (granulomatosis with polyangitis/Wegeners)
pANCA positive vasculitis
MP (microscopic polyangitis)
EGPA (eosinophilic granulomatosis with polyangitis/Churg-Strauss)
Signs/symptoms of ANCA associated vasculitis
Fever, polymyalgia, polyarthralgia, headache, malaise, anorexia, weight loss
Nasal obstruction/ulcers/discharge/crusting, epistaxis, sinusitis
Cough, haemoptysis, pleuritis
Ulcers, papules, nodules, palpable purpura
Keratitis, conjuncitivitis, scleritis, episcleritis, uveitis, retinal vessel occlusion, optic neuritis
Mononeuritis multiplex
Nephritic syndrome
Types of cystic renal disease
ADPKD ARPKD Simple cysts Acquired renal cystic disease Von Hippel Lindau disease
Extra-renal complications of ADPKD
Berry aneurysms - SAH!! Hepatic/pancreatic cysts Spleen cysts Mitral valve prolapse Diverticuli
Presentation of ADPKD
Early hypertension (around age 20)
Vague abdominal/loin discomfort with a palpable mass (often bilateral)
Acute pain or renal colic may be due to cyst rupture
Haematuria
UTI
CKD
Causes of raised albumin/protein:creatinine ratio
Glomerulonephritis
Diabetes
Amyloidosis
Myeloma
Causes of haematuria
Malignancy (KUB) Calculi IgA nephropathy Glomerulonephritis Polycystic kidney disease Alport syndrome
What counts as a lower UTI
Cystitis
Prostatitis
What counts as an upper UTI
Pyelonephritis
What does a ‘complicated’ UTI mean
UTI in the presence of a structural/functional abnormality of the genitourinary tract e.g. obstruction, catheter, stones, neurogenic bladder, renal transplant
Symptoms of cystitis
Frequency Dysuria Urgency Suprapubic pain Polyuria Haematuria
Symptoms of acute pyelonephritis
Fever Rigor Vomiting Loin pain/tenderness Costovertebral pain Associated cystitis symptoms Septic shock
Symptoms of prostatitis
Pain in the perineum/rectum/scrotum/penis/bladder/lower back Fever Malaise Nausea Urinary sx Swollen/tender on PR exam
Management of UTI in a non-pregnant woman
If 3+ symptoms/1 severe of cystitis and no vaginal discharge then treat empirically with 3 day course of trimethoprim/nitrofurantoin
If first line fails culture urine
If upper UTI do urine culture and start broad spec antibiotics
Management of UTI in pregnant women
Can cause preterm delivery and IUGR
If asymptomatic bacteruria do a second sample
Treat with antibiotic
Avoid Ciprofloxacin/Trimethoprim in the first trimester
Avoid Nitrofurantoin in the third trimester
Management of UTI in men
If lower UTI then 7 day course of trimethoprim/nitrofurantoin
If prostatitis then long (4wk) course Ciprofloxacin
If upper or recurrent UTI then urology referral
Signs of hypovolaemia
Low BP Low UO Non-visible JVP Poor tissue turgor Fast pulse Daily weight loss
Signs of fluid overload
High BP Raised JVP Lung crepitations Peripheral oedema Gallop rhythm
When do you treat hyperkalaemia
> 6.5 or with any ECG changes (do an ECG on anyone with K >6)
How long does renal disease need to be present for to classify as CKD
> 3 months
BP target for CKD patients; a) without DM b) with DM
a) <140/90
b) <130/80
Three things that can go wrong with an AV fistula
Thrombosis
Stenosis
Steal syndrome
When would you use haemofiltration rather than haemodialysis
When the patient is really haemodynamically unstable (low BP, critical care ect)
Contraindications to renal transplant
Absolute: cancer with metastates
Temporary: active infection, HIV with viral replication, unstable CVD
Relative: congestive heart failure, CVD
Factors contributing to renal transplant loss
Donor factors - age, comorbidity, living/deceased, donor after brain death vs cardiac death Rejection Infection BP/CVD Recurrent renal disease in graft
Presentation of IgA nephropathy
Asymptomatic microscopic haematuria or episodic visible haematuria, high BP, proteinuria
Presentation of HSP
Purpuric rash on extensor surfaces typically on the legs, polyarthritis, abdominal pain (GI bleeding), nephritis
Presentation of post-streptococcal glomerulonephritis
Around 2 weeks after throat infection or 3-6 weeks after skin infection
Haematuria, nephritis, oedema, high BP, oliguria
Presentation of anti-GBM disease (Goodpasteurs)
Renal disease - oliguria/anuria, haematuria, AKI, renal failure
Lung disease - pulmonary haemorrhage, SOB, haemoptysis
Signs and symptoms of hypernatraemia
Lethargy Thirst Weakness Irritability Confusion Signs of dehydration Coma Fits
Causes of hypernatraemia
Usually due to loss of fluid > loss of Na
Diarrhoea/vomiting/burns
Diabetes insipidus
Primary hyperaldosteronism
Iatrogenic from fluids (excessive saline)
Signs and symptoms of hyponatraemia
Anorexia, nausea, malaise
Headache, irritability, confusion, weakness, dropping GCS, seizures
Cardiac failure/oedema depending on cause
Low Na is an important cause of falls in the elderly
Causes of hyponatraemia
Dehydrated;
Urinary Na >20 means sodium and fluid is being lost from the kidneys - Addisons disease, renal failure, too many diuretics, osmotic diuresis (high glucose or urea)
Urinary Na <20 means sodium and fluid is being lost elsewhere - diarrhoea, vomiting, fistulae, burns, small bowel obstruction, trauma, heat exposure, trauma
Not dehydrated;
Oedematous - nephrotic syndrome, cardiac failure, liver cirrhosis, renal failure
Not oedematous but urine osmolality >100 - SIADH
Not oedematous but urine osmolality <100 - water overload, severe hypothyroidism, glucocorticoid insufficiency
Concerning signs and symptoms of hyperkalaemia
Fast irregular pulse Chest pain Weakness Palpitations Light-headedness
Causes of hyperkalaemia
Oliguric renal failure Addisons disease K-sparing diuretics Rhabdomyolysis Metabolic acidosis (DM)
Signs and symptoms of hypokalaemia
Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, arrythmias (can cause light-headedness), constipation
ECG changes in hypokalaemia
Small or inverted T waves
Prominent U waves
Long PR interval
ST depression
Causes of hypokalaemia
Diuretics Cushings syndrome/steroids/ACTH Vomiting/diarrhoea Pyloric stenosis Conn's syndrome
Signs and symptoms of hypercalcaemia
'Bones, stones, groans and psychic moans' Abdo pain, vomiting, constipation Polyuria, polydipsia Depression, anorexia, weight loss, tiredness, weakness HTN Confusion, pyrexia Renal stones, renal failure Low QT interval
Causes of hypercalcaemia
Malignancy! (bone mets, PTHrP, myeloma)
Primary hyperparathyroidism
Sarcoidosis
Lithium
Signs and symptoms of hypocalcaemia
'SPASMODIC' pneumonic Spasms (Trosseaus sign, Chvosteks sign) Peri-oral paraesthesia Anxious/irritable/irrational Seizures Muscle tone increased in smooth muscle causing colic, wheeze, dysphagia Orientation impaired/confusion Dermatitis Impetigo herpetiformis Cardiomyopathy (long QT interval)
Causes of hypocalcaemia
CKD
Hypoparathyroidism
Low Mg
Low vitD
What causes haemolytic uraemic syndrome?
It is a thrombotic microangiopathy
Usually 5-10 days after bloody diarrhoea in children - Usually caused by toxins from enterohaemorrhagic E.coli which damage endothelium (vessels and glomeruli) and cause microthrombi formation. Get haemolysis because of small vessel blockage by thrombi.
What 2 extra blood tests can you do to assess for haemolysis and would they be high or low
High LDH
Low Haptoglobin
What is the triad of haemolytic uraemic syndrome
- Low platelets - petechia, purpura, mucosal bleeding
- Microangiopathic haemolytic anaemia - fatigue, dyspnoea, pallor, jaundice
- Decreased renal function - haematuria, proteinuria, oliguria/anuria
What is the pentad of thrombotic thrombocytopenic purpura
- Microangiopathic haemolytic anaemia - fatigue, pallor, jaundice
- Low platelets
- AKI
- Neurological symptoms - headache, palsies, seizure, confusion, coma
- Fever
How does autosomal recessive PCKD present
Ante/perinatally with renal cysts (salt and pepper appearance on USS), congenital hepatic fibrosis and portal hypertension
Features of Alport syndrome
Progressive renal insufficiency
High-tone sensorineural hearing loss
Visual changes - anterior lenticonus, bulging of lens seen on slit lamp examination
Causes of cystic kidney disease
Multicystic dysplastic kidneys (congenital) ADPKD/ARPKD Simple cysts Acquired cysts Tuberous sclerosis Von Hippel Lindau Medullary cystic kidney disease
