renal Flashcards
what happens to urine osmolality and urine sodium in pre-renal disease
- K still ftns to concentrate urine and retain sodium
- urine osmolality HIGH >500 mOsm/kg
- urine sodium LOW
mx of hyperkalaemia
BNF - If K+ > 6.5 mmol/l or if there are ECG changes:
1.Administer 10 ml 10% CALCIUM GLUCONATE by slow IV injection titrated to ECG response
2.Give 10 U ACTRAPID in 50 ml of 50% GLUCOSE over 10-15 MINS
2.Consider use of nebulised salbutamol
4.Consider correcting acidosis with sodium bicarbonate infusion
Nb. to remove potassium from body –> calcium resonium, loop diuretics, dialysis
HLA matching for renal transplant what is most imp
DR>B>A
RF for AKI
- CKD
- Other organ failure/chronic disease eg HF, liver failure, DM
- hx of AKI
- use of drugs with nephrotoxic potential eg NSAIDs, aminoglycosides, ACEi, ARBs + Diuretics in past week
- use of iodinated contrast agents in the past week
- age 65Y+
Drugs safe to continue in AKI
- paracetamol
- warfarin
- statins
- aspirin (at CARDIOPROTECTIVE DOSE 75mg od)
- clopi
- beta blockers
drugs that should be stopped in AKI as may worsen renal function
- NSAIDs (except aspirin at 75mg)
- Aminogylcosides
- ACEi
- ARB
- Diuretics
drugs that may need to be stopped in AKI as increased risk of toxicity (but won’t WORSEN AKI itself)
Metformin - stop if eGFR <45ml/min due to risk of lactic acidosis
Lithium
DIgoxin
Adult PKD extra renal features
Extra-renal manifestations
- LIVER CYSTS (70% - the commonest extra-renal manifestation): may cause hepatomegaly
- BERRY ANEURYSMS (8%): rupture can cause SAH
- CV system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
- CYSTS in OTHER ORGANS: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
what is the max rate of potassium infusion via peripheral line
10 mmol / hour
-rates above 20 mmol / hour require cardiac monitoring
gold std for bladder cancer diagnossi
CYSTOSCOPY
-recommended in all pts with sx suggestive of bladder C
KDIGO criteria stage 1
- Increase in creatinine to 1.5-1.9 times baseline, or
- Increase in creatinine by ≥26.5 µmol/L, or
- Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
KDIGO criteria stage 3
1.Increase in creatinine to ≥ 3.0 times baseline, or
2.Increase in creatinine to ≥353.6 µmol/L or
3.Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
4.The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
what happens in acute tubular necrosis to urine osmolality and urine sodium
ATN = most common cause of renal AKI
- the K no longer FTNs to concentrate urine + retain sodium SO –>
- urine osmolality LOW
- urine sodium HIGH
how is post renal AKI identified usually
due to obstruction of urinary tract –> identified with hydronephrosis on renal US
what rate should maintenance fluids be prescribed
30 ml/kg/24h
diabetic nephropathy screening
- all pts screened anually using ACR
- early morning specimen
- ACR>2.5 = microalbuminuria
diabetic nephropathy mx
- dietary protein restriction
- tight glycaemic control
- BP aim for <130/80
- ACEi or ARB should be started if ACR of 3mg/mmol +
- control dyslipidaemia eg statins
4x causes of transient or spurious non-visible haematuria
1-UTI
2-menstruation
3-vigorous exercise (this normally settles after around 3 days)
4-sexual intercourse
causes of persistent, non-visible haematuria
- cancer (bladder , renal, prostate)
- stones
- BPH
- prostatitis
- urethritis e.g. Chlamydia
- renal causes: IgA nephropathy, thin basement membrane disease
spurious causes of red/orange urine, where blood is not present on dipstick
foods - beetroot, rhubarb
drugs - rifampicin, doxorubicin
what is the definition of non-visible haematuria
microscopic or dipstick positive haematuria
-found in 2.5% population
painless visible haematuria is most likely whata
TCC of bladder
urgent referral 2WW to urology
age >45Y +
- unexplained visible haematuria without UTI, or
- visible haematuria that persists or recurs after successful tx of UTI
age>60Y +
-have unexplained non-visible haematuria + either dysuria or a raised WCC on bloods
non-urgent referral to urology indications
age >60Y with recurretn or persistent unexplained UTI
-since the Ix (or not) of non-visible haematuria is so common, in general –> pts <40Y with normal renal ftn, no proteinuria + who are normotensive DO NOT need to be referred + may be Mx in primary care
what happens to anion gap in DKA, septic shock + methanol poisoning
RAISED
- as they lead to dev of anion that is not incl in calclulation of anion gap
- Septic shock –> lactic acidosis
- DKA –> raised ketones
- methanol poisoning –> rise in formic acid
alport syndrome inheritance + features
X-linked dominant pattern
- MICROSCOPIC HAEMATURIA
- PROGRESSIVE RENAL FAILURE
- bilateral SN DEAFNESS
- LENTICONUS: protrusion of the lens surface into the anterior chamber
- RETINITIS PIGMENTOSA
- RENAL BIOPSY: splitting of -lamina densa seen on electron microscopy
what is the screening test for PCKD
Ultrasound scan
CKD 2x basic problems
- 1 alpha hydroxylation normally occurs in the Kidneys –> CKD leads to LOW VIT D
- Kidneys normally excrete phosphate –> CKD leads to HIGH PHOSPHATE
CKD 3x further problems due to low vit D + high phosphate
1-high phosphate levels ‘drags’ calcium from the bones –> OSTEOMALACIA
2-LOW CALCIUM: due to lack of Vit D, high phosphate
3-SECONDARY HYPERPARATHYROIDISM: due to low calcium, high phosphate + low vit D
how to mx high phosphate in CKD
=aim is to reduce phosphate and parathyroid hormone levels.
1-reduced dietary intake of phosphate is the 1st-line mx
2-phosphate binders
3-vitamin D: alfacalcidol, calcitriol
4-parathyroidectomy may be needed in some cases
PHOSPHATE BINDERS =aluminium-based binders are less comm used now
=Ca-based binders
problems include hypercalcemia + vasc calcification
=sevelamer
a non-calcium based binder
what type of DI can hereditary haemochromatosis cause
CRANIAL DI
what happens in urea: creatinine ration in pre renal disease
RAISED serum urea: creatinine ratio
HSP prognosis
usu excellent with full renal recovery, esp in children without renal invovlement
-around 1/3 pts have relapses
mnemonic for kidney functions x 7
A - WET - BED Acid-base balance Water balance Electrolyte disturbance Toxin removal BP control EPO production Vitamin D metabolism
Mx of CKD - based on ftns x5
- Modify RF - antihypetensives, good glycaemic control
- FLUID BALANCE - fluid + salt restriction
- ANAEMIA - EPO stimulating agents
- HYPOCALCAEMIA - phosphate binders, activated Vit D replacement (alpha calcidol)
- RRT - PD, HD, Renal transplant - for stage 5 disease (eGFR<15)
Cx of AV fistula
Pain, infection, bleeding
Thrombosis, stenosis, aneurysm, steal syndrome, high output HF
Cx of Tesio line
Sepsis, PERITONITIS, DIC, Fluid overload, DDS = cerebral oedema
