renal Flashcards
classification of CKD
proteinuria?
earliest expression of diabetic nephropathy?
microalbuminuria
how to differentiate between pre-renal failure and intrinsic renal damage
functions of kindey
maintain water + electoclyte balance
acid-base balance
excrete waste products (urea + creatinine)
produces erythropoetin adn renin
function of proximal covoluted tubule?
loop of henle?
distal convoluted tubule?
PCT = reabsorbs 100% glucose, proteins, carbohydrates
* 70% Na+ and H2O
Loop of Henle = creates hypeosmotic environment in medulla
DCT = reabsorbs water, Na+ and bicarbnate, excretes K+ and H+
epithelial cells lining glomerular capallaries?
glomerular filter?
podocytes
glomerular filter = enodthelium of capillary + basement membrane + pedicels of podocytes
blood supply to renal medulla?
vasa recta
hormone that acts on DCT?
ALDOSTERONE
increases reabsorption of Na+ thus water, increasing BP
what hormone acts on collecting ducts?
ADH - increases water reabsoprtion
structures lined by transitional epihtelium (urothelium)?
features
mior calyx, major calyx, ureter, bladder
cells of luminal surface called umbrella cells because domed
urethra of female vs male
female 3-5cm
* lined by trnasitional epithelium which transitions to stratified squamous
male 20cm
* prostatic urethra (from bladder through prostate) - transitional epithelium
* membranous (from prostate to bulb of penis) - transitional changes to straified columnar
* penile urethra - changes to stratified squamous
osmolarity of body fluids
300 mosmol/l
body water components
ICF = 70%
ECF = 30%
* ECF = plasma (20%), interstitial fluid (80%), lymph
how to calculate body fluid compartments
TBW = ICF + ECF
tracer for ECF = inulin
TBW = H2O
ICF = TBW - ECF
ionic concentrations of ICF vs ECF
osmotic concentratiosn of ECF vs ICF
IDENTICAL 300 mosmol/l
extracellular K+?
>95% of K+ is intracellular
leakages can cause
* muscle weakness + paralysis
* arrhythmias and cardaic arrest
regulation of renal blood flow thus GFR
extrinsic = sympathetic via baroreceptor reflex
intrinsic = myogenic + tubuloglomerular feedback
if capillary blood pressure falls…
GFR will decrease
kidney response to haemorrhage
mucula densa cell function?
sense NaCl content of tubular fluid
high levels = constriction of afferent arterioles
other determinants of glomerular filtration rate
plasma clearance of inulin? - what is used instead
glucose?
what is used to calculate renal plasma flow?
inulin = GFR (creatinine used clinically)
glucose = 0
para-amino hippuric acid (PAH) used to calculate renal plasma flow
accelerated hypertension?
medical emergency
diastolic BP >120 mmHg
papilloedema
encephalopathy, fits, cardiac failure, acute renal failure
leukonychia?
splinter haemorrhages?
leukonychia seen in nephrotic syndrome - low albumin
splinter haemorrhages - CKD, vasculitis
UTI urinalysis
leukocytes + nitrites
normal 24 hour urine?
normal P:CR
grading proteinuria
normal 24 hour = <150mg/24 hours
urine protein:creatinine = 0.5g/24 hours
asymptomatic low grade = PCR <1g/day
heavy proteinuria = PCR 1-3 g/day
nephrotic = PCR >3g/day
ACR >30 = proteinuria
what does this show?
LVH!!
(probably severe hypertension)
what does this show?
hyperkalaemia - tall teneted T waves
Acute kidney injury?
classifcation?
An abrupt (<48 hrs) reduction in kidney function defined as:
- Increase in serum creatinine by >26.4umol/l (50%)
- Reduction in UO
nephrotic syndrome triad?
proteinuria >3g/day
hypoaluminaemia
oedema
nephritic syndrome symptoms?
AKI
oliguria
oedema/fluid retention
hypertension
active urinary sediment - RBCs (haematuria), leukocytes
risk factors AKI?
older age
CKD
Diabetes
Cardiac failure
Liver disease
PVD
Previous AKI
Also – hypotension, hypovolaemia, sepsis, deteriorating NEWS, recent contrast, exposure to certain medications
Ax pre-renal AKI?
Tx?
pre-renal AKI (commonest cause of AKI in hopsital - sepsis + severe dehydration)
- hypovolaemia = haemorrhage, burns
- hypotension = cardiogenic shock, sepsis, anapylaxis
- renal hypoperfusion = NSAIDs, ACEI, hepatorenal syndrome, rhadbomyolysis
Tx = fluid challenge for hypovolaemia (NaCL, NOT dextrose)
Ax AKI?
pre-renal
renal
post-renal
untreated pre-renal AKI?
leads to tubular necrosis
Ax renal AKI?
Vascular
- Vasculitis, renovascular disease
Glomerular
- Glomerulonephritis
Interstitial nephritis
- Drugs - antibiotics e.g. penicillin
- Infection (TB)
- Systemic (sarcoid)
Tubular injury
- Ischaemia
- Drugs (gentamicin)
- Contrast
- Rhabdomyolysis
s/s renal AKI?
Anorexia, weight loss, fatigue
N + V
Itch
Fluid overload – oedema, SOB
Signs
- Fluid overload – hypertension, oedema, pul oedema, effusions
- Uraemia – itch, pericarditis
- Oliguria
clues to cause of renal AKI?
History e.g. sore throat (antibiotics), rash (vasculitis), joint pains, D + V, haemoptysis
Recent contrast
Drugs
Bloods – eosinophilia, CK
Vascular bruits
Dx renal AKI?
obviously increase in serum creatinine >26.4 (50%)
+ reduction in UO
in addition:
- U + Es (hyperkalaemia)
- FBC + coagulation (abnormal clotting, anaemia, CK)
- urinalysis (haematoproteinuria)
- USS (?obstruction)
- immunology - ANA, ANCA, GBM
Tx renal AKI?
Stop nephrotoxics
Establish good perfusion pressure – fluid resuscitiate (if no improvement = inotropes, vasopressors)
Treat underlying cause
Dialysis if no urine passage
life threatening complications AKI?
Hyperkalaemia
Fluid overload (pulmonary oedema)
Severe acidosis (pH <7.15)
uraemic pericardial effusion
severe uraemia (>40)
post-renal AKI Ax?
Tx?
Obstruction of urine flow leading to back pressure (hydronephrosis)
Ax = Stones, cancer, strictures, BPH
Tx = relieve obstruction, catheter/nephrostomy
life threatening hyperkalaemia?
signs?
Tx?
Life threatening hyperkalemia = >6.5
signs = muscle weakness, T waves on ECG
Tx = calicum gluconate (to protect myocardium), then insulin with 50% dextrose (move K+ back into cells), then calcium resonium (to stop GI absoprtion)
urgent indications for dialysis?
Hyperkalaemia >7 ( or >6.5 unresponsive to therapy)
Sever acidosis pH <7.15
Fluid overload
Urea >40, pericardial rub/effusion
ECG changes hyperkalaemia?
medicines to stop on sick days?
ACE-I and ARBS
NSAIDs
diuretics
metformin + empagliflozin
1 = goodpasture’s syndrome
2 = rhabdomyolysis?
3 = acute tubular necrosis?
4 = obstructive uropathy
furosemide
calcium gluconate
elevated creatinine
kidneys reabsorb….
99% of fluid
99% of salt
100% of glucose
100% of amino acids
50% of urea
0% creatinine
proximal tubule absoprtion + secretion?
fluid is?
Reabsorbed in PT
- 70% Na (via K+ATPase) + water
- 100% glucose + amino acid
- phosphate, sulphate, lactate
Secreted in PT
- H+, neurotransmitters, bile pigments, uric acid, drugs, toxins
fluid is iso-osmitic (~300) in PT
Loop of Henle function?
physiology
formation of hypertonic urine
entire loop functions as countercurrent multiplier
together the loop and vasa recta establish a hyper-osmotic medullary interstitial fluid
ascending vs descending limb loop of henle?
CKD Dx?
complications?
CKD requires 2 samples at least 90 days apart
comps = AKI, falls, fragility
stages CKD?
ACR CKD?
golden rules of CKD?
Monitor people for development/progression of CKD for at least 2-3 years after AKI, EVEN IF serum creatinine has returned to baseline
Advise people who have had AKI that they are at increased risk of CKD
accelerated progression CKD?
risk factors associated wtih CKD progression?
Sustained decrease in GFR of >25% within 12 months
OR
Sustained decrease in GFR of 15/ml/min per year
risk factors = CVD, AKI, hypertension, diabetes, smoking, chronic use of NSAIDs, untreated urinary outflow obstruction, African/Asian origin
people with CKD who should be referred for specialist assessment?
GFR <30 (G4 + 5)
ACR >70
ACR >30 with haematuria
sustained decrease of GFR by 25% in 12 months
poorly controlled hypertension
suspected renal artery stenosis
blood pressure targets CKD?
In people with CKD, aim to keep <140/90
In people with CKD and diabetes, keep <130/80
CKD Tx?
ACE-I/ARB
atorvastatin 20mg
alfacalcidol, phosphate binders, calcimimetic for CKD-MBD
iron therapy for anaemia
Ax CKD?
clinical signs CKD?
Anaemia – conjunctival + palmar pallor
Weight loss
Advanced uraemia
- Lemon yellow
- Uraemic frost
- Twitching
- Encephalopathic flap
- Confusion
- Pericardial rub/effusion
- Kussmaul breathing (metabolic acidosis)
symptoms CKD?
Uraemic
- N + V
- Anorexia
- Weight loss
- Fatigue
- Itch
- Altered taste
- Restless legs
- Muscle twitching
- Difficulties concentrating
- Confusion
Thirst
Anaemia = fatigue, muscle weakness
Pain = bony, neuropathic, ischaemic, visceral
consequences CKD?
Renal
- Pain, haemorrhage, infection
- Haematuria, proteinuria
- Impaired salt and water handling
- Hypertension
- Electrolyte abnormalities
- Acid-base disturbance (metabolic acidosis)
- ESRD
Extra-renal
- CVD
- Mineral and bone disease (extra PTH, calcium moved from inside bones)
- Anaemia
- Malnutrition
ESRD Tx?
dialysis
transplant
CVD in CKD?
Starts early – eGFR <50
Risk increases with microalbuminuria even if eGFR normal
Tx CKD-mineral bone disease
Phosphate restriction
Salt reduction
Potassium restriction
Fluid restriction
meds = alfacalcidol, phosphate binders (aluminium), calcimimetic (Cinacalcet)
renal anaemia?
Target?
renal anemia = HB <100 despite no iron deficiencies
target Hb = 100-120g/l
autosomal dominant polycystic renal disease Ax?
significance?
S/s?
extra-renal features?
Mutation in PKD1 gene
Important cause of ESRD!!
s/s = chronic pain (back), hypertension, haematuria (cyst rupture etc), cyst infection, renal failure
extra-renal:
- hepatic cysts
- intra-cranial aneurysms!!
- cardiac valvular disease
- abdominal/inguinal hernias
Dx ADPKD?
USS = cysts + renal enlargement
CT/MRI
genetics - PKD1
ADPKD genetic counselling?
Offspring of affected individual 50% risk of having disease
Tx ADPKD?
Tolvaptan!
control BP
if progressed to renal failure = dialysis + transplant
autosomal recessive PKD affects?
gene?
cysts where?
S/s?
children - associated with hepatic lesions
gene = PKDH1 on chromosome 6
cysts bilateral + symmetrical, collecting ducts!
S/s
- kidneys always palpable
- hypertension
- recurrent UTI
Alport’s syndrome?
S/s?
Dx?
Tx?
X-linked herediatary nephritis
S/s = haematuria, sensorineural deafness, anterior lenticonus, leiomyoma of oesophagus/genitalia
Dx = suspect in haematuria + hearing loss
renal biopsy characteristic feature = variable GMB thickness
Tx = no specific treatment, treat BP, maybe dialysis/transplant
Anderson Farby’s disease clinical features?
Dx?
Tx?
features = renal failure, angiokeratomas, cardiomyopathy + valve disease, stroke, acroparaesthesia
Dx = plasma a-GAL, renal biopsy
Tx = enzyme replacement - fabryzyme
medullary cystic kidney?
difference from ADPKD?
Dx?
Tx?
autosomal dominant
difference from ADPKD = normal sized/small kindeys (in ARPKD and ADPKD kidneys are enlarged + palpable)
Dx = family history + CT scan
Tx = renal transplant
medullary sponge kidney?
sporadic inheritance - medulla looks like a sponge
fluid in loop of henle?
Tubular fluid leaving loop of Henle entering distal convoluted tubule is hypo-osmotic to plasma
hormones controlling fluid + electolyte balance?
ADH = increased water reabsorption (collecting duct)
Aldosterone = increased Na reabsorption, increased H+/K+ secretion (DCT)
Atrial natriuretic hormone = decreased Na reabsorption
Parathyroid hormone (PTH) = increased calcium reabsorption, decreased phosphate reabsorption
distal tubule fluid?
permeability?
segments?
Tubular fluid is hypo-osmotic to plasma
Distal tubule has LOW permeability to water and urea
Distal tubule can be described as 2 segments (early + late)
- Early = NaCl reabsorption
- Late = Ca, Na, K reabsorption (except K+ is secreted in presence of aldosterone) + H+ secretion
high ADH?
low ADH?
High ADH = high water permability + hypertonic urine
Low ADH = low water permeability + hypotonic urine
diabetes insipidus s/s?
Tx?
s/s = large volumes of dilute urine + constant thirst
Tx = ADH replacement
ADH release?
hypothalamic osmoreceptors!!! = most important
also stimulated by decreased left atrial pressure = increased ADH
GI stretch receptors = inhibits ADH
nicotine stimulates ADH, alcohol inhibits
aldosterone released by?
when?
function?
aldosterone secreted by adrenal cortex
secreted in response to rising K+ or falling Na+ in the blood
OR activation of RAAS
stimulates Na+ reabsorption and K+ secretion in DCT
effect of aldosterone?
Normally 90% of K+ is reabsorbed in proximal tubule
When aldosterone absent, the rest is reabsorbed in the distal tubule (therefore, no K+ excreted in urine)
An increase in [k+] directly stimulates adrenal cortex
Aldosterone stimulates secretion of K+ in distal tubule
A decrease in plasma [Na+] promotes indirect secretion of aldosterone
triggers for renin release from JGA?
reduced pressure in afferent arteriole
macula densa cells (decreased NaCl)
reduced arterial blood pressure
what is responsible for fluid retention in congestive heart failure?
Tx?
RAAS
Tx = low salt diet, loop diuretics + ACE-I
Atrial natriuretic peptide?
Heart produces ANP which is stored in atrial muscle cells
ANP released when cells mechanically stretched due to increase in circulating plasma volume
ANP promotes excretion of Na+ and diuresis
Lowers BP :))
micturation controlled by?
Micturition reflex
- Stretch receptors in bladder wall initiate micturition reflex
- Bladder contraction and opening of internal and external urethral sphincters
Voluntary control
- Tightening of external sphincter and surrounding pelvic diaphragm
aldosterone summary
pH of artrial vs venous blood?
increase in [H+]?
pH of arterial blood = 7.45
pH of venous blood = 7.35
An increase in H+ REDUCES pH
complication of acidosis?
alkalosis?
acidosis = depression of CNS
alkalosis = overexcitability of PNS and then CNS
most important physiological buffer
what is the most common cause of ESRD?
2nd most common?
most common = diabetes
2nd most common = chronic glomerulonephritis
what is glomerulonephritis?
Immune-mediated disease affecting glomeruli
clinical presentation glomerulonephritis?
Damage to endothelial or mesangial cells leads to proliferative lesion + red cells in urine
Damage to podocytes leads to non-proliferative lesion and protein in urine