Renal Flashcards by Laura Lazzari

What are causes of AKI

Pre-Renal (most likely approx 70%): hypoperfusion

hypovolaemia (bleeding, shock, dehydration)
Oedema (cardiac /liver failure, nephrotic syndrome
Renal hypoperfusion (renal artery stenosis, vasculitis, drugs)

Renal: intrinsic kidney damage, classified on location (vasculitis, glomerulonephritis, tubular, interstitial)

Post-Renal: obstruction to urinary flow (calculi, tumours, strictures, BPH)

How well did you know this?

Not at all

Perfectly

what are A>E findings for AKI

A.	Vomiting
B.	Tachypnoea, cough (pulmonary oedema), bibasal crackles
C.	Tachycardia, fluid overload
D.	Confusion (uraemia), oliguria
E.	Abdominal pain (retention)

How well did you know this?

Not at all

Perfectly

what is workup for AKI

•	Bedside: ECG (hyperkalaemia), urine dipstick, urine sample (MC&S, ACR), ABG (acidosis, hyperk)
•	Bloods: U&E, calcium, phosphate, FBC, CRP/ESR, LFTs, CK (for rhabdo), renal screen
•	Imaging: bladder scan, renal uss
Renal biopsy (if unsure of cause - rarely done)

How well did you know this?

Not at all

Perfectly

What is management for AKI

• Treat HYPERKALAEMIA
o 10-30mL Calcium Gluconate IV over 2-10 mins (can repeat every 15 mins up to 5 doses until K+ corrected) (N.B. IV calcium gluconate must be administered by a dr due to risk of arrhythmia)
o 10 U Actrapid with 100mL 20% glucose IV over 10 mins
o Consider 5 mg Salbutamol nebuliser
o Monitor ECG and ensure quick access to defibrillator
o Repeat U&E
o ABG to check for acidosis

Review drugs - stop drugs that reduce renal perfusion (NSAIDS) are nephrotoxic (aminoglycosides) are renally escreted (metforming) can cause hyperk (ACEi/ARB)

Fluid resus
Catheterise, monitor UO
Treat the CAUSE
o Hypovolaemia > IV fluids
o Retention > catheterise
o Pulmonary oedema > cautious use of furosemide

How well did you know this?

Not at all

Perfectly

What are indications for dialysis

Acidosis (refractory to treatment / severe <7.2)
Electrolyte imbalance (refractory hyperkalaemia)
Intoxication (CKD stage 5; GFR <15)
Oedema pulmonary /overload of fluid
Uraemia complications (encepalopathy, nausea, pruritus, pericarditis)

How well did you know this?

Not at all

Perfectly

How can you define AKI

KDIGO guidelines:

increase serum creat >26 within 48hours
increase serum creat >1.5x baseline within past 7 days
urine vol <0.5ml/kg/h for 6 hours

How well did you know this?

Not at all

Perfectly

How can you classify AKI

Based on creatinine compared to baseline or based on URINE OUTPUT

How well did you know this?

Not at all

Perfectly

What is presentation of AKI

oliguria / anuria
dehyrdation, thirst, dry mouth 
confusion 
uraemia: malaise, nausea, vomiting, pruritus, drowsiness 
hypotension, hypovolaemia (if prerenal) 
palpable bladder (if postrenal) 
renal bruits (if renovasc disease)
dehydration

How well did you know this?

Not at all

Perfectly

What are two blood markers of renal function

Urea

Creatitinine

How well did you know this?

Not at all

Perfectly

What is creatinine

breakdown of protein metabolism within muscles

How well did you know this?

Not at all

Perfectly

How does creatinine travel through kidneys

creatinine enters the blood

is freely filtered through kidneys

How well did you know this?

Not at all

Perfectly

what pathology can alter creatinine amount in the blood

and why

Creatinine is produced and excreted through kidneys at constant rate

So if RENAL FUNCTION DECREASES

You reduce creatinine excretion > increased in creatinine in blood

How well did you know this?

Not at all

Perfectly

what is eGFR

Serum creatinine + age + sex + ethnicity

How well did you know this?

Not at all

Perfectly

What is creatinine clearance

eGFR + height + weight

How well did you know this?

Not at all

Perfectly

why is creatinine clearance importannt

because the amount of creatinine produceed is dependent on our muscle mass

How well did you know this?

Not at all

Perfectly

What is urea

a nitrogenous waste product

How well did you know this?

Not at all

Perfectly

what conditions can cause urea to be elevated in the blood

DEHYDRATION - as urea is reabsorbed by kidneys when dehydrated

UGI BLEED - as RBC breakdown cause increased urea

How well did you know this?

Not at all

Perfectly

What is classification of AKI

KDIGO stages 1-3
Stage1: serum creatinine 1.5 to 1.9x reference; bodyweight in urine mLs every 2 hours for <12 hours
Stage 2: serum creatinine 2.0 to 2.9x reference; bodyweight in urine mLs every 2 hours for over 12 hours
Stage 3: serum creat >3; anuric >12h

How well did you know this?

Not at all

Perfectly

Drugs that need to be stopped in AKI

DAMN

Diuretics
ACEi, ARB
Metformin
NSAID

How well did you know this?

Not at all

Perfectly

What are three forms of renal replacement therapy

Haemodialysis
Peritoneal dialysis
Renal transplant

How well did you know this?

Not at all

Perfectly

How does peritoneal dialysis work

Peritoneum is used as semipermeable membrane. Dialisate is instilled in peritneum

How well did you know this?

Not at all

Perfectly

What is advantage and disadvantage of peritoneal dialysis

Advantage: can be done at home
Disadvantage: risk of infection

How well did you know this?

Not at all

Perfectly

Explain how haemodialysis works

Access via AV fistula / tesio
Takes blood out, passes it through dialysate. It is separated from dialysate via a semipermeable membrane
Electrolyte imbalances are corrected via diffusion; fluid overload is corrected via negative pressure in the dialysate (draws out water from blood=)

How well did you know this?

Not at all

Perfectly

What are problems that occur with renal failure (link back to the specific renal function)?

Fluid balance&raquo_space; FLuid overload
Electrolyte homeostasis&raquo_space; hyperkalaemia, acidosis
Waste excretion&raquo_space; uraemia
Hormone production&raquo_space; anaemia, hypercalcaemia (hyperphosphataemia)

How well did you know this?

Not at all

Perfectly

Ix for CKD

``` UE blood glucose K+ FBC Antibodies, USS, biopsy ```

stages of CKD

1: eGFR >90 2: eGFR >60 3: eGFR >30 4. eGFR >15 5. eGFR <15

How do you manage CKD

1. modify RF => antihypertensives, good dlycaemic control) 2. fluid balance => restrict fluid + salt 3. Anaemia => EPOstimulating agents 4. hypocalcaemia => phosphate binders, vit D supplements 5. consider renal replacement therapy

Nephritic syndrome triad

BPH Blood (Haematuria) proteinuria Hypertension

What are causes of nephritic syndrome

Immune-mediated - IgA nephropathy - Post strep glomerulonephriitis - Henoch Schonein , HUS, SLE, Goodpastures CAUSE INFLAMMATION OF GLOMEROLUS AND NEPHRON > CAPILLARY BECOMES LEAKY

Describe what occurs in IgA nephropathy

Following resp/GI infection Abnormal IgA is produced Immune system makes antibodies against it Sticky immune complexes are produced

Explain how IgA nephropathy presents

5-7 days post infection | Abdo pain, rash, arthritis

Explain how Post-Strep Glomerulonephritis presents

4-6 weeks post infection

What must you manage in Post-Strep Glomerulonephritis

HTN

what is triad of nephrotic syndrome

PHO Proteinuria Hypoalbuminaemia Oedema + Thrombosis (due to loss of antithrombin III thhrough kidneys)

Causes of nephrotic syndrome

Minimal change diisease FOcal segmenral glomerulonephritis (MOST COMON) Membranous glomerulonephritis

what are causes of CKD

``` long term renal injury usually linked to: - DM -HTN - chronic inflammation (glomeerulonephritis, vasculitis, myeloma, amyloidosis) ```

what is mode of inheritance for PKD

Autoomal dominant

what occurs in PKD

multiple renal cysts develop and cause damage to adjacent nephrons

how and when does PKD present

in > 30 years old liver cysts: flank pain, haematuria, HTN berry aneurysm: SAH Mitral valve prolapse

HOw can you manage PKD

give TOLVAPTAN to slow down progression

what is the usual cause of RAS

atherosclerosis

what occurs to renal enzymes in RAS

Renal hypoperfusion> increased angiotensin 2, increased aldosterone > increased BP

whhat drug is AWFUL if you have RAS and wy

ACEi because in RAS renal perfusion is actually maintained by constriction of the efferent arteriole ACEi remove that constriction > glomerular filtration pressure drops > little blood flows to kidey > severe AKI

Gold standard Ix for RAS

Digital subtraction angiography

WHAT IS fibromuscular dysplasia

Proliferation of cells in the walls of the arteries causing the vessels to bulge or narrow. This most commonly affects YOUNG WOMEN Susceptible to AKI after the initiation of an ACE inhibitor. On MR angio: 'string of beads' appearance.

What are stimuli for renin secretion

low Na low perfusion sympathetic stimulation (beta adrenergic receptors)

how does renin act on the RAS

Renin releasedd from JGA | Renin converts angiotensinogen to Angiotensin 1

What occurs to angiotenssin 1

Angiotensin 1 is cleaved in lung by ACE to At2

What is function of At2

Stimulates adrenal production of aldosterone | also constricts arterioles

how do you distinguish glomerulonephritis from AIN on urine dip

glomerulonephritis = NEPHRITIC syndrome = blood and protein in urine AIN = NePHROTIC syndrome = protein and WCC

what do you do if a patient has CKD but needs a scan with contrast?

give IV saline before and after - this reduces the risk of precipitating an AKi

what CK levels are you expecting for rhabdomyolysis

CK >10 000 otherwise (if lower than that) it could just be a soft tissue injury

what histopathological findings do you expect with a carcinoma

nuclear enlargement hyperchromasia pleomorphism

difference between IgA and post infection nephropathy in terms of timing

IgAA is FEW DAYS | post-infectious is FEW WEEKS

How does urinary sodium differ between prerenal and renal AKI, and why?

prerenal: LOW urinary sodium because the kidney works fine and is desperately trying to hold on to sodium to raise BP renal: HIGH urinary sodium because the kidney is damaged so loses lots of sodium

classify and name causes or intrinsic renal AKI

VASCULITIS - affects the blood vessels - small vessels (microangiopathic): HUS, TTP, DIC, GPA - large vessel (obstructive): renal artery / vein thrombosis or embolus GLOMERULONEPHRITIS - affects the glomerolus - minimal change disease (in children) - membranous glomerulonephritis (in adults) ATN - affects tubules - rhabdomyolisis, post-hypovolaemia AIN - affects intersttium - NSAIDS, PENICILLIN, SULFA-DRUGS, PPI, CIPROFLOX, ALLOPURINOL, FUROSEMIEDE

most common extarenal presentation of PKD

cystic liver > hepatomegaly

what is a dangerous unique complication of haemodysalisis

Dialysis disequilibrium syndrome | causes cerebral oedema (headache, drowsiness)

why do you need to STOP LITHIUM in AKI?

because may cause toxic accumulation of lithium (although lithium itself does not actually cause AKI)

what dose of aspirin can you continue for AKI

low dose (75 mg)

how do you treat cranial DI

DESMOPRESSIN

how do you treat nephrogenic DI

thiazide

when does a GP need to refer to nephrology someone with CKD

if; - eGFR below 30 - eGFR falls progressively by > 15 in a year

what else other than GFR do you need to diagnose CKD stages 1 and 2

you need supportive evidence (e.g. from urine dip, USS, symptoms) otherwise likely not CKD, as GFR is simply variable in peoopke

what dose of potassium is safe to give IV per hour WITHOUT CARDIAC MONITORING

10mmol / h

what must a patient be on if receiving 20mmol KCl /h

requires cardiac monitoring | via central line preferred

what is the pathophysiology of goodpasture

anti-GBM antibodies against T4 collagen

what are symptoms of goodpasture

pulmonary haemorrhage > haemoptisis | glomerulonephritis > NEPHRITIC syndrome (proteinuria + haemoaturia)

how much does creatininee need to increase by to recognise an AKI

>26 micromol / L

what are the three ways of removing potassium from the body (rather than merely shifting it into cells) in hyperkalaemia

calcium resonium (enema > oral) loop diuretics dialysis

what electrolyte imbalance can large volumes of NaCL cause

hyperchloraemic metabolic acidosis

which vit D supplement is good for end stage kidney disease a

alpha calcidiol