Renal Flashcards
About how much is GFR
120 ml/min/1.73m2
What is creatinine?
Chemical waste product from muscle metabolism
What can cause a misleadign creatinine level ?
Extreme muscle mass e.g. cachexia/body builder = misleading
Why is creatinine clearance > GfR
Secreted as well as filtered
[Therefore inhibitors of secretion will make Cr rise and function look worse e.g. trimethoprim]
3 hormones in Na excretion and therefore volume control
Aldosterone (adrenal) -> decreased excretion
Angiotensin II -> decreased excretion
ANP - released by heart in response to high pressure -> increases excretion
In kidney which hormone dilates afferent arteriole? constricts?
Prostaglandin
Angiotensin II
[angi is a bit constrictive - the bitch]
Name 2 SEs od ACEi
May impair renal function: decrease GFR (avoid NSAIDs), hyperkalaemia (avoid K+ spare diuretics)
Postural hypotension
Bradykinin mediated dry cough
Fatigue
Name an ARB and 2 SEs
Losartan
Renal impairment
Postural hypotension
Hyperkalaemia
Name 1 med causing hypo K and 1 causing hyper K
Hypokalaemia meds
Loop diuretics, thiazide diuretics
Hyperkalaemia meds
Spironolactone, amiloride, ACEI, ARB
Key transporter in loop of henle
NKCC2:
Na K Cl Cotransporter (energy dependent)
Where do ADH and aldosterone take effect on?
Distal convoluted tubule and collecting duct
Barter’s syndrome .. same as?
When?
2 features
Effect of loop diuretics
Children
Metabolic alkalosis
Low Mg
High urinary Ca
[C’s - Children, [loop=Circle], high Ca]
Gitelmans syndrom same as?
age?
2 features?
same effect as Thiazide diuretic (Distal convoluted tubule)
Late childhood
Mg decreased, urine calcium normal/low,
Metabolic alkalosis
What does renal tubular acidosis result in?
Hyperchloraemic metabolic acidosis
+ hypobicarbonataemia + decreased arterial pH
+ normal anion gap
2 Most common cause of renal tubular acidosis
fanconi syndrome
drug induced
What happens in fanconi syndrome
Generalised dysfunction of renal proximal tubule ->
urinary loss of bicarb, [glucose, aa, phosphate, peptides, organic acids. ]
Leads to salt wasting and volume depletion
Name 2 Rfs for RTA
Childhood, urinary tract obstruction, DM, [stones, adrenal insufficiency]
Name 3 ways RTA could present?
Growth retardation/failure to thrive (children)
Muscle weakness (Fanconi)
Hypoglycaemia after fructose
Rickets (Fanconi and Type 2 proximal have persistent phosphate loss)
Kussmaul breathing if severe
2 key findings from Ix in RTA? name another one
Low serum bicarbonate
serum anion gap normal (12-18)
[high serum chloride, variable potassium, arterial pH low, ]
Mx of RTA
if Hyperkalaemia + mineralocorticoid deficiency?
Sodium alkali
Fludrocortisone + dietary restriction of potassium
Mx of Hyperkalaemia + mineralocorticoid deficiency
in RTA
Fludrocortisone + dietary restriction of potassium
Name 2 comps of RTA
volume depetion (due to loss of Na)
Nephrocalcinosis - due to bone buffering of acidosis
Osteoperosis - due to bone buffering of acidosis
Grow retardation - acidosis -> muscle catabolism
Renal rickets - in fanconi
2 Causes of end stage renal failure
Glomerulonephritis
Pyelonephritis
Diabetes
PKD
Usual cause and bugs for pyelonephritis
Escherichia coli, UPEC
[diabetes/HIV/malignancy/transplant - think candida/klebsiella]
ascending from lower urinary tract or spread hematogenously to kidney
Name 3 RFs for severe pyelonephritis
Extremes of age
anatomical abnormality
foreign body
Immunocmpromised
obstruction
pregnant
Cause of pyelonephritis only found in men
prostatitis and BPH cause urethral blockage -> bacteriuria -> pyelonephritis
Triad of presentation in pyelonephritis
Loin pain
Fever - may not be the case if patient is on steroids or anti-inflammatory
Renal tenderness/costovertebral angle
Name 3 Ix in pyelonephritis
Imaging
- Renal USS:
- Contrast CT
Urine dip:
Urinalysis (microscopy) WBC
Gram stain:
Urine culture:
FBC: leukocytosis
ESR/CRP raised
Blood culture (systemic infection SEPSIS)
Seen on gram stain in pyelonephritis
G -ve rods (e.coli, klebsiella, proteus)
Mx of mild.mod pyelonephritis ?
Severe/comp/pregnant?
Ciprofloxacin PO BD
Severe: Admit to hospital IV ceftriaxone / cipro/gent IV fluids IV paracetamol Catheterisation if compromised
Name 2 comps of pyelo
Renal failure, abscess formation, parenchymal renal scarring, recurrent UTIs
2 main types of renal cell carcinoma
80% clear cell/adeno renal carcinoma
15% papillary tumour
3 RCC RFs
smoking, obesity and hypertension
Occupational exposure to some chemicals such as asbestos, cadmium, lead, chlorinated solvents, petrochemicals
VHL
Usual pres of RCC
asymptomatic and diagnosed incidentally
3 key are:
abdo mass + haematuria + loin pain
Which genetic cause increases risk of RCC
Von hippel lindau
AD
Principles of Ix in RCC…Name 3?
Check kidney function
Check for structure
Check for metastasis
=
Percutaneous renal biopsy
*FBC - polycythaemia (EPO)
LDH - raised is poor prognosis
Corrected calcium - >2.5 mmol/l poor prognosis
LFT - raised AST/ALT = metastatic disease
*Cr - elevated with reduced clearance
Urinalysis - haematuria and/or proteinuria
- Abdominal/pelvis USS - cyst, mass, mets
- CT abdo/pelvis - lymphadenopathy, mass, bone mets inc contralateral kidney
MRI - for local invasion etc
CXR - cannonball metastasis, bone scan, MRI brain/spine
Main comp of RCC? Name 1 other
Paraneoplastic syndrome (30% of patients) - anaemia
[Hypercalcaemia, SIADH]
Mx of RCC?
Surgical
= partial / laparoscopic nephrectomy
What could you use in late stage RCC
tyrosine kinase inhibitor = first line e.g. SUNITINIB
Childhood renal tumour
Wilm’s tumour -> nephroblastoma
What is AKI
An acute decline in *GFR from baseline/increase in creatinine with or without oliguria
Name 4 causes of AKI
Pre-renal (50%)
Azotaemia
Renovascular disease
Intrarenal 30% Acute tubular necrosis (mainly due to sepsis = most common) *Rapidly progressive glomerulonephritis *Interstitial nephritis Vascular disease
Post renal 20%
Mechanical obstruction to urinary tract
Retroperitoneal fibrosis, lymphoma, tumour, prostate hyperplasia, renal calculi, urinary retention, pyelonephritis
What is azotaemia> features?
high nitrogen compounds e.g. Ur, Cr) due to reduced perfusion
hypovolaemia, haemorrhage, sepsis
Which pt can you not give NSAIDS? why?
giving NSAIDs to patient with bilateral renal artery stenosis
-> renovascular disease
Most common cause of AKI
Acute tubular necrosis
[Acute - AKI
FSG - Glomerulonephritis - in the names]
Name 3 nephrotoxic drugs
CANT DAMAG
Contrast, antibiotics (penicillin/ceph), NSAIDs, Therapeutic index (narrow), diuretics, ACEI, metformin, ARB, gentamicin
What is used to measure stage of AKI
Creatinine
Urine output
3 Ix in AKI - if anuric which is a priority
U+E+Cr:
*Elevated creatinine, *high serum potassium (or on *VBG), *metabolic acidosis
Urine dip, MC + S
Infection -> leukocytes/nitrates
Glomerular disease -> blood/protein
FBC
Anaemia (CKD/blood loss), leukocytosis (infx), thrombocytopenia (HUS, TTP)
Imaging *priority if anuric
Renal USS -> obstruction, cysts, mass
*ECG
For *hyperkalaemia - increased PR, widened QRS, peaked T, sine wave
Ratio serum urea:creatinine + other tests of cause
AKI mx ... 3 basic things? Raised K ix? Obstruction Ix? Severe?
Stop nephrotoxic drugs
ABCDE
Including fluid challenge if hypotensive, diuretic if hypertensive
Catheterise for accurate urine output
K
Urgent VBG/ABG + ECG
Obstruction
Urgent USS KUB
Dialysis If uraemic, severe metabolic acidosis, severe hyperkalaemia
What is CKD
Proteinuria or haematuria (evidence of kidney damage) and/or reduction in GFR to <60ml/min/1.73m2 for more than 3 months
2 causes of CKD
DM and HTN (+AI disorder, smoking, obesity)
Mx of CKD (think of cause)
Glycaemic control for diabetic nephropathy and optimisation of BP
Stages of CKD
GFR
1 >90 2<60 3a <45 3b<30 4<15 5>15
Primary prevention CKD ?
Secondary?
DM - HbA1c < 7%,
HTN - BP < 140/90,
smoking cessation, BMI < 27
As above +
salt restriction + protein restriction
3 parts of the uraemic syndrome presentation (GFR<15)
Uraemic tinge (grey/yellow) Nausea/vomiting Itch *Uraemic encephalopathy *Pericarditis *Bleeding For RRT
Name 3 comps of CKD
anaemia (less epo)
osteodystrophy
(low Ca / vit D)
CV disease
Protein loss
Hyper K
Metabolic acidosis
Pulm oedema
3 Ix in CKD
Serum creatinine elevated
Urinalysis: haematuria or proteinuria
Urine microalbumin: microalbuminuria
Renal USS: small kidney, obstruction/hydronephrosis, large kidney (infiltration myeloma, amyloidosis)
eGFR < 60
Blood sugar
FBC - anaemia, normochromic normocytic
Osteodystrophy: hypocalcaemia, hyperphosphataemia and hyperparathyroidism, high alkaline phosphatase
Antibodies
Mx of CKD General Anaemia Bone disease Metabolic acidosis oedema HyperK
How to restrict uraemia?
Treat reversible causes - obstruction / drugs
Glycaemic control
BP/CV risk - ACEI/ARB
[Statin, smoking cessation, weight loss, aspirin]
Educate about RRT at stage 3/4
Treat anaemia Epoeitin alfa (EPO stimulating agent)
Treat renal bone disease Dietary modification (based on Ca and PO4 - milk, cheese, eggs) ± calcitriol if low
Treat metabolic acidosis
Oral sodium bicarbonate
Treat oedema
Loop diuretics and restrict sodium
High potassium
Low potassium diet
Low protein diet to restrict uraemia
2 main options of Mx at stage 5 CKD
RRT:
dialysis / transplant
Give 2 indications for RRT in AKI
Uraemia (pericarditis, gastritis, encephalopathy)
Pulmonary oedema (fluid retention) unresponsive med Rx
Severe hyperkalaemia (>6.5) unresponsive to med Rx
Severe hypo/hypernatramia
Severe metabolic acidosis (<7.0) unresponsive to bicarb
Severe renal failure (urea > 30)
How does haemodialysis work
Blood passed over semi-permeable membrane against dialysis fluid (opposite direction)
Blood meets less concentrated solution and small solutes may diffuse along concentration gradient
Blood drawn from AV fistula, heparin constantly infused
Name 3 comps of haemodialysis
Access: *infection, thrombosis, aneurysm, endocarditis, stenosis
*Hypotension (common), cardiac arrhythmia, air emboli
Nausea, vomiting, headache, cramps
- Anaphylaxis to sterilising agent
- Disequilibration syndrome: restless, tremor, fits, coma
How does peritoneal dialysis work?
Dialysate infused into peritoneal cavity, uses blood in peritoneal capillaries
Waste collected below (gravity)
Ultrafiltration controlled by altering osmolality to draw water out of blood (e.g. glucose)
2 comps of peritoneal dialysis
Infection: peritonitis
Catheter problems: infection, blockage, leak
Constipation, fluid retention, hyperglycaemia + wt gain
Hernia
Name 2 advantages of transplant over dialysis
Survival, QoL, economic, enable pregnancy, reversal of anaemia and renal bone disease
2 Technical challenges with transplant
Retrieving kidney, storing (cold storage), implanting
Long term immunosupressive agents for renal transplant
prednisolone,
calcineurin inhibitors (tacrolimus/ciclosporin)
anti-metabolites (azathioprine
Name 2 CIs for renal transplant in CKD
active infection, uncontrolled IHD, AIDS
Name 4 comps with renal transplant
Immediate operative: local infx, pain, DVT
Infections due to immunosuppression (viral HSV for 4 weeks then CMV, bact, fungal)
Urinary tract obstruction
Drug toxicity: bone marrow suppression
- Cancer (skin, lymphoma)
- CV disease (main cause of death), hypertension, dyslipidaemia
Rejection
Disease recurrence
Name the types of rejection and how long after surgery you’d expect
Hyperacute (mins),
rare due to crossmatch
Accelerated (days),
T cell mediated crisis -> fever, swollen kidney, increased Cr -> IV steroids
Acute cellular (weeks), 25% in <3 weeks -> fluid retention, rising BP, rising Cr, high dose IV steroids
Chronic (years),
gradual rise in Cr and proteinuria, resistant HTN -> graft biopsy shows vascular changes, fibrosis and atrophy (non-responsive to immunosuppression)
Most common cause of glomerulonephritis
Focal segmental glomerulonephritis in nephrotic syndrome
Which is proliferative Nephrotic / nepritic?
2 causes of each
Nephritic = proliferative [Nephritic is prolific] IgA nephropathy (1ary) Postinfectious GN (1ary) Rapidly progressive GN: -Vasculitis -Anti-GBM GN
Nephrotic = non-proliferative Deposition disease (amyloidosis + light chain dep) Minimal change disease Focal and segmental GN Membranous nephropathy Membranoproliferative GN
Signs of nephrotic
Proteinuria (>3.5g/24 hours)
Hypoalbuminaemia (<30g/L)
Peripheral oedema
Hyperlipidaemia
Signs of nephritic
Oliguria/AKI (renal dysfunction)
HTN
Haematuria: active urinary sediment (red cells and casts)
Usual cause of nephrotic in children?
Cause?
Seen on light microscopy / immunoflourescence/ electron microscopy?
Minimal change disease
-Idiopathic, NSAIDs or Hodgkin’s lymphoma
Light microscopy - normal glomeruli
Immunofluorescence - no immune complex deposition
Electron microscopy - effacement of podocyte foot processes
Minimal change Mx
steroids
Usual cause of nephrotic in younger adults ? Cause?
seen on light microscopy?
focal segmental glomerulosclerosis
-Idiopathic or secondary to HIV
Light microscopy - segmental areas of mesangial collapse and sclerosis
Most common cause of nephrotic in adult / older ?
seen on light microscopy / immunoflorescence?
Membranous nephropathy
-Usually idiopathic or secondary to Hep B, gold, penicillamine, NSAIDs
Light microscopy - basement membrane thickening and associated cellular proliferation
Immunofluorescence - granular IgG deposition
Name 2 secondary causes of nephrotic syndrome
diabetes, amyloidosis, SLE, infection, drugs Eg NSAIDS, Gold, penicillamine
Name 2 DDx of nephrotic
CCF (increased JVP, pulmonary oedema, oedema)
Liver disease (decreased albumin)
Name 3 comps of nephrotic
Susceptibility to infection - increased urinary loss of IgG (streptococcal), or secondary to steroids
Hypercoagubility and thromboembolism - renal vein thrombosis (lupus or urinary loss of antithrombin III, altered protein C and S)
Hypercholesterolaemia - increased hepatic lipoprotein synthesis and loss of lipid regulating proteins
Hypocalcaemia - loss of vit D in urine
Hypervolaemia - severe decrease in GFR resulting in oedema
AKI - more likely with acute GN
HTN - impaired GFR and increased reabsorption of salt and water
What is nephritic syndrome
acute kidney injury with rapid deterioration in function
Most common cause of nephritic syndrome - what happens?
buerger’s disease
Macroscopic haematuria 24/48 hours post GI/URTI
IgA deposition in mesangial matrix
2 causes of nephritic syndrome
Buerger’s
Membranoproliferative
Post infection
Rapidly progressive glomerulonephritis
- Goodpasture
- Wegners
- Microscopic polyangitis
Glomerulonephritis presents with RFs + haematuria + oedema + HTN + oliguria+
What do these extra Sx indicate?
Anorexia/nauseas -
Weight loss
Fever
Skin rash
Arthralgia
Abdo pain
Haemoptysis
Anorexia/nauseas -> vasculitic
Weight loss -> systemic
Fever -> infectious aetiology
Skin rash -> vasculitic
Arthralgia -> vasculitic
Abdo pain -> HSP and post-streptococcal glomerulonephritis
Haemoptysis -> in anti-glomerular basement membrane disease and Wegener’s
Name 3 Ix in glomerulonephritis
FBC - anaemia -> systemic
U + E + Cr + LFT -> ?hepatitis, advanced disease, albumin
Urinalysis -> haematuria, proteinuria, RBC casts
GFR -> normal or reduced
Lipid profile + glucose
24 hour urine collection
Renal biopsy and light or electron + immunofluorescence micros
Hep B/C/HIV serology
Antibody testing
Electrophoresis
In glomerulonephritis what would these things indicate
ESR
Complement - low
RF
ANCA -
Anti GBM antibody
Antistreptolysin O antibody/anti DNase -
Anti DS DNA/ANA
Electrophoresis - raised gamma globulin
ESR - vasculitis
Complement - low in immune complex
RF - RA
ANCA - wegners
Anti GBM antibody - anti-GBM disease or Goodpasture’s
Antistreptolysin O antibody/anti DNase - post strep
Anti DS DNA/ANA - SLE
Electrophoresis - raised gamma globulin in lymphoma and amyloidosis
Mx of post strep glomerulonephritis
IM BenPen
Mx of mild glomerulonephritis - (isolated haematuria, normal GFR)
antibiotics/ antivirals/ withdraw drug
*limit salt + fluid
Mx of mod/severe glomerlonephritis (haematuria, proteinuria and reduced GFR) ?
What if nephrotic?
ACEI/ARB), + ABX + furosemide + prednisolone
[FAAP]
immunosuppressant e.g. cyclophosphamide
Mx of antiGBM glomerulonephritis
plasma exchange (remove aB) + IV methylprednisolone + IV cyclophos
Mx of immune complex glomerulonephritis
IV methylpred
Mx of Lupus nephritis
IV methylprednisolone + cyclophosphamide
you get AD and AR PKD… Name 2 comps
HTN, increased CV morbidity, CKD, ruptured intracranial aneurysm, ESRD
What is the protein involved in PKD
polycystin
What is this
Patients often present in the neonatal period with enlarged echogenic kidneys, renal cysts congenital hepatic fibrosis.
ARPKD
High mortality - probs gonna die by teens
Name 3 sx/signs on presentation of PKD
Name 3 other places that get cysts
FHx of PKD/ESRD or stroke
Flank/abdominal discomfort due to enlarging kidneys, haemorrhage or stone formation
Lumbar pain (females) Haematuria (males)
HTN (at 20-35) **** -> mandatory screening with renal USS
DUFS (infection, UTI)
Palpable kidneys
Headaches (intracranial aneurysm)
Hepatomegaly (liver)
Cystic locations - Liver (80%), pancreas (10%), seminal vesicles (40%), brain (10%)
PKD Ix
Renal USS
Genetic - PKD1/2
CT abdo pelvis
Relevant further testing
- Urinalysis (protein, bacteria)
- ECG - LVH +
- echo - aortic root dilation
- MR (Magnetic resonance) angiography - screen for aneurysm
Family screening in PKD
Screen for SAH in 1st degree relatives of those with ADPKD with MR angiography
Mx of infection with PKD eg of UTI or of cyst
ciprofloxacin
PKD How to limit fluid secretion into cysts?
How to target cell proliferation
*Target fluid secretion-
Calcium mimetics - cinacalcet
CFTR inhibitors
Metformin
*Target cell proliferation -
Somatostatin
Name 4 causes of glomerulonephritis
Idiopathic
Infection - eg strep pyogenes
Systemic
-SLE, RA, Wegners, HUS, HSP, Goodpastures
Drugs
-Penicillamine, NSAIDS, ciclosporin
Metabolic
-HTN, diabetes
Other
-Alports, Lung / bowel Ca, amyloidosis
Types of RTA
1 - distal
- Cant excrete H+ in distal tubules
- > Raised urine pH = stones
- low/normal potassium
2-Proximal
- Cant reabsorb bicarb
- > low urine pH
- low normal potassium
4 - distal
- in aldosterone deficiency
- HYPERKALAEMIA
- Low urine pH
- High serum bicarb
Faconi
liddles syndrome? metabolics
opposite effect to potassium sparing diuretics
[liddle different - opposite effect]
Hypertension, hypokalaemia
Metabolic alkalosis
[Acts at ENaC, Autosomal dominant]
CKD comps
Nervous
Peripheral neuropathy
Restless leg
tiredness / fatigue (urea)
CV
Fluid overload
ACCELERATED ATHEROGENESIS
Pericarditis
GI
altered taste
reduced Ca absorption
Bone
Hyperparathyroidism
-Osteodystrophy
Electrolyte
Hyper K
Acidosis
Blood
reduced EPO - anaemia of chronic disease
Impaired platelet function
Mx of CKD groups
Conservative Education Planning for dialysis Fluid RESTRICTION diet - avoid K and PO4
Medical CV risk factors EPO Bicarbonate cinacalcet to reduce PTH
Interventional
Renal replacement therapy
Mnemonic for Ix in renal
[AND FOR EVERY SPECIALITY]
[Cant Believe I Look Fresh]
Cultures
-Urinalysis + culture
Bloods
Arterial - ABG
Venous - K, Urea+creatinine, Antibodies, lipids
LFTs
Imaging
CXR, AXR
USS
Scope / biopsy [looking]
Biopsy
Functional (specific)
ECG
