Renal Flashcards
Give 3 common causes of CKD
- renovascular disease
- hypertension
- diabetes
- glomerular nephritis (nephrotic and nephritic syndromes)
- Hereditary diseases like APCKD
less common causes in autoimmune disease (SLE), myeloma etc
What are the 3 classic findings in nephrotic syndrome?
- high cholesterol
- gross protein urea (causes frothy urine)
- Low serum albumin
How does nephrotic syndrome usually present?
- pitting odema in legs
- odema in face worse in morning
- any age
- predisposing factor eg diabetes, fhx
- frothy urine
- incidental finding of gross protein urea
Give 3 secondary causes of nephrotic syndrome?
- diabetes
- lupus nephritis
- myeloma
- amyloid
- pre- eclampsia
give 3 primary causes of nephrotic syndrome
- FSGS
- minimal change
- membranous nephropathy
What are the classical findings of nephritic syndrome?
- blood and small amounts of protein in urine
- no swelling
- vague symptoms
How may CKD present?
- vague symptoms like fatigue, malaise, anorexia, weakness
- swelling of face and legs
- breathlessness due to pulmonary odema
- pruritis, lethargy, cramps and headaches due to raised urea
- insomnia
- polyurea
- sexual dysfunction
- predisposing factors often present
- usually picked up incidentally by urine dips
How is CKD investigated?
- urine dip
- 24 hr urine collection/ spot urine collection to look at ACR
- bloods: u&e, alk phos, parathyroid hormone, plasma glucose and HbA1c, serum ablumin, lipid screen (usually high), FBC (normocytic anaemia), anti nuclear antibodies, serum free light chains, c ANCA and p ANCA, anti GMB if no clear cause
- ECG and echo as heart failure is often a differential and LVH often occurs due to fluid overload
- Renal USS if suspect APCKD, obsutruction, haematuria, low GFR
- renal biopsy when indicated
When should a renal biopsy be done in someone with CKD
Progressive disease, nephrotic syndrome, systemic disease, AKI without recovery, unknown cause
When should the GP refer someone with CKD to a nephrologist?
- When reach stage 4
- ACR>70 mg/mmol unless due to DM
- ACR >30 with haematuria
- eGFR decrease by 15% in 12 months or >25% total
- high BP poorly controlled despite >4 antihypertensives at theraputic dose
- known or suspected rare or genetic cause of CKD
Describe stage 1-5 CKD
1= eGFR> 90 2= 60-89 3= 30-59 4= 15-29 5= <15
List 5 complications of CKD
- hypertension
- odema
- hyperkalaemia
- uremia
- coagulopathies
- acidosis
- anaemia of chronic disease
- hypocalcamia with hyperparathyroidism
- rugger jersey spine/mineral bone disease (related to above)
- CVD due to high BP, vascular stiffness, inflammation, oxidative stress, abnormal endothelial function
What treatment is given in CKD to slow disease progression
- ACEi or ARB (not both) and check K+ before and 2 weeks after starting treatment
- Good glyaemic control
- lifestyle advice
- Avoid NSAIDS, nephrotoxic drugs and K+ sparing diuretics (amiloride and spironolactone)
- Adjust doses of renal metabolised/ excreted drugs
What treatments are given for CKD complications?
- odema: furosemide/ bumetanide, restrict sodium and fluid intake
- Anaemia: ferrous sulphate or IV iron then EPO if not work
- Acidosis: sodium bicarb supplements
- high phosphate and K+: reduce in diet (refer to dietician), calcium acetate works as phosphate binder
- hyperparathyoidism/ hypocalcaemia: give adcal D3/ alphacalciferol
- CVD: anti platelets (aspirin) and statin
Describe the management of hyperkalaemia? inc doses
- Do ECG and VBG to confirm
- If K+> 6.5 or ECG changes, give IV calcium gluconate 10mg 10% over 10 mins and actrapid 10 units and 50mls 50% dextrose immediately
- Also give calcium resonium (15-45mg) to bind the Ca2+
- Give 5-10mg salbutamol neb if K+ not coming down
- sodium bicarb and call renal reg if still refractory
- Final option is dialysis
- If k+ 6-6.5 or no ECG changes, give calcium gluconate usually, stop K+ sparing diuretics, give fluids/ hydrate, think about loop diuretics if refractory
Give 2 pre renal, 2 renal and 2 post renal causes of AKI
Pre: hypovolaemia, sepsis, cardiac failure, renal artery occlusion, renal vein thrombosis
Renal: small vessel vasculitis, glomerular disease (anti GBM, lupus), ATN (ischaemia, nephrotoxins, rhabdomylosis) acute interstitial nephritis (drugs, infection)
Post: calculi, retroperitoneal fibrosis, bladder outlet obstuction (tumour)
What are the 3 criteria for AKI?
- Rise in serum creatinine of > 26 umol/L over 48hrs
- 50% or greater increase in creatinine within 7 days
- fall in urine output to less than 0.5 ml/kg/hr for more than 6 hrs
What investigations would you do for suspected AKI?
Urinalysis: dipstick for blood, nitrates, leukocytes, glucose, osmolality
Bloods: FBC, Blood film, U&Es, coag studies (DIC), CK, myoglobinurea (?rhabdomyalysis), autoantibody screen virology
USS when ?obstruction
CXR- pulmonary odema, AXR- renal calculi
Doppler USS to look for stenosis or renal arteries and veins
How is AKI managed?
- monitor fluid and electrolyte balance closely
- treat cause
- pre renal aki: fluid replacment
- withdraw nephrotoxic drugs
- identify and treat complications (hyperalaemia, acidosis, pulmonary odema, bleeding)
- restrict oral K+ and monitor carefully
When should renal replacement therapy be used in AKI? (6)
- Hyperkalaemia (>6.5) refractory to medical management
- pulmonary odema/ fluid overload refractory to medical management
- metabolic acidosis refractory to medical therapy
- uraemia complications (pericarditis or uraemic encephalopathy)
- CKD stage 4/5
- dialysable nephrotoxin
- intrinsic renal disease (vasculitis, GN, SLE) suspected
When does a pt with CKD need specialist renal care? (7)
- GFR < 30 with or without diabetes (stage 4)
- ACR 70 or more unless diabetes
- ACR 30 or less with haematuria
- sustained decrease in GFR or 25% or more
- Hypertension which remains poorly controlled despite 4 drugs at theraputic doses
- known or suspected rare or genetic causes of CKD
- Suspected renal artery stenosis
- outflow obstruction should go to urology
Describe how youd undertake a fluid assessment?
look at tongue, JVP, skin turgor, HR,RR BP, cap refill, pulmonary odema, peripheral odema
Give adv and dis avd of haemodialysis
Disadv: need to go in hospital 4x 3 hrs a week, need access with central line or fistula, diet restrictions
Adv: can sometimes be done at home, other hrs of week they can do as please, can remove fluid at same time,
What are the two types of peritoneal dialysis
APD: nightime bags
CAPD: continuous bags
The more concentrated the bags the more fluid is removed
What are contraindications of peritoneal dialysis
IBD, adhesions due to previous abdo surgery, massive central obesity or very little abdofat
What 3 drugs does everyone go on after renal transplant
Tacrolimus, azathioprine and cyclosporin
Most also go on mycophenolate and prednisolone. Also need contraception for 1st year and need to monitor U&E, dipstick, PTH, lipids, glucose and screen for malignancies.
What are the advantages of renal transplant
no diet restriction, normal life afterwards
What are the complications of haemo and peritoneal dialysis?
peritoneal: peritonitis, thickening of peritoneum leading to small bowel obstruction (encapsulating peritoneal sclerosis) or access failure
Haemo: fistula clotting, SVC obstuction, endocarditis, line sepsis, access failure, shock
Give 3 complications of renal transplants
infections, rejection, obstuction, thrombosis, delayed graft function, donor derived infections , graft vs host disease, new onset diabetes after transplant, malignancies, damage during operatiion
What may cause nephritic syndrome (7)? Give a couple of secondary features associated with each
- ANCA/ small vessel vasculitis (churgg strauss, wengers- rashes, asthma, joint pain)
- IgA nephropathy (gross haematuria, after infections or strenuous exersize)
- Anti GBM (pulmonary haemorrhage)
- Think basement membrane disease (hereditary)
- Alport (hearing and eye problems)
- Post Step GN (1-2 weeks after impetigo/ tonsilitis)
- Lupus
How is IgA nephropathy diagnosed and managed?
- increased serum IgA, intermittent visible/ microscopic haematuria and mesangeal immune complex deposition in glomeruli on biopsy
- treatment is with immmunosurpression, give an ACEi for HTN
How is ANCA vasculitis diagnosed and managed?
- +ve c ANCA (GPA) or p ANCA (churgg strauss, MPA)
- immunosurpression
How is ANTI GBM diagnosed and managed?
- +ve anti GBM autoantibodies + biopsy and pulmonary infiltrates on CXR
- manage with immunosurpression and plasma exchange
How is alport syndrome diagnosed and managed?
alternative thickening and thinning of GBM and sensorineural hearing loss
management is supportive
What is the normal anion gap and what is the equation?
(Na + K) - (cl + HCO3)
Normal gap is 8-12
What is the anion gap useful for?
Determining cause of metabolic acidosis - increased acid or decreased alkali?
What does a high anion gap suggest?
Increase in organic acids- as it means unmeasured ions make up a greater proportion of the anions in the serum.
Organic acids inc lactic acid, ketoacids, methanol or ethanol poisioning, can be due to renal failure also
What does metabolic acidosis with a normal anion gap suggest?
acidosis is due to decrease in alkali
- renal loss of bicarb (RTA, addisons)
- diarrhoea (loss of Cl-)
How much K+ does a patient need per day and what’s the fastest you can give it?
1mmol/kg/day (for maintanance- increased if vomiting or high output stoma)
Dont give faster than 10mmol/hr, if faster than 20mmol/hr need cardiac monitoring.
If in AKI, they need more fluid and less K+.
(if K+ consistently low, check Mg)
Why shouldnt you give too much saline?
lots of Na and CL!! can get hyperchloarmic acidosis which will lead to reduced eGFR
how should nephortic syndrome be managed
- fluid restriction, furosemide +/- thiazide to reduce odema- monitor body weight
- treat cause (usually steroids)
- ACEi/ ARB reduces proteinuria
- identify/ prevent/ manage complications (VTE, infection, hyperkalaemia, hyper lipidaemia)
