A top notch renal referral includes 5 things… sCr measurements over time, urine dip, fluid status assessment, urine output and BP measurements….without these, we’ll get you to call us back…
eGFR values in AKI aren’t helpful or accurate…use serum creatinine
sCr goes up in between HD sessions and down after HD, as does serum K+…serum K will rebound quickly after so no need to give K supplements/IV KCl
Think of an HD patient as a ‘closed tank’ that’s emptied by HD…giving fluid and electrolytes risks pulmonary oedema and hyperkalaemia..!
Protect, protect, protect residual renal function in PD/HD patients…each residual working nephron counts towards survival…
The haemodialysis unit is not the safest place for a sick, drowsy, confused or bleeding patient – call us before sending them there
Years of life is lost with each loss of access…so don’t be tempted to take bloods from that dialysis line, fish around that fistula arm during the pheb round or stick a urometer on that PD catheter…
Drowsy CKD/dialysis patient…I bet they’re taking a high dose of…Gabapentin? Pregabalin?…remember to use the lowest dose and up-titrate
Acyclovir, Baclofen and Certain Antibiotics (penicillins, cephalosporins, carbepenems, quinolones) all cause encephalopathy or neurotoxicity – so reduce dose accordingly…we’ve all seen ‘that’ ITU admission…
Don’t diagnose AKI if taking Trimethoprim/Co-Trimoxazole/Cimetidine…stop the drug first and the sCr should come down and hyperkalaemia go away (increases tubular creatinine secretion and blocks ENaC channels)…but don’t forget to treat the high K (increased risk of sudden death in these drugs…)
You’re patient’s confusion is very unlikely to be because of the urea of 20….try at least double that, often even treble…
Don’t assume that acidosis is due to ‘renal failure’ – always check lactate, glucose and ketones at a bare minimum and calculate the anion gap…
No opiates are ‘safe’ but, if all other analgesic options fail…prescribe the lowest dose, avoid slow/prolonged release preparations and try oxynorm, hydromorphone, fentanyl patch/lozenge as options (but watch for toxicity!)
Check a VBG K+ to rule out pseudohyperkalaemia
Sine waves on ECG?…what’s their K+?…Heart block?…what’s their K+?…ST changes?…what’s their K+?…bradycardia/VF/VT…what’s their K+? I’d rather have insulin/dextrose to fix my arrhythmia than being paced until someone checks my U+E…
Sodium bicarbonate….severe hypocalcaemia, fluid overload, worsens acidosis by CO2 retention in drowsy/COPD, reduces oxygen affinity…it is not risk free so don’t shell it out, check with us first
Ampules of 8.4% (hypertonic) sodium bicarbonate…has no effect on serum K+…osmolar drag from hypertonic solution pulls water out of cells and brings K+ along with it…if need to use for hyperkalaemia – use 1.26%
Don’t diagnose AKI without checking the baseline sCr first…especially as mountains of IV fluid won’t restore chronically damaged nephrons in CKD
NOT ALL AKI IS PRE-RENAL…litres of fluid won’t help if the patient is oedematous or even euvolaemic…look for other causes (image renal tract and do urine dip)
A urine dip is GOLD to us…if there is protein and/or blood on it – rule out infection, do a renal screen and let us know!!.. as your AKI/progressive CKD is likely to be due to an intrinsic cause and the patient my need a kidney biopsy…
AKI in an older male is obstruction until proven otherwise…
Catheterisation is not necessary to monitor fluid balance – a bedpan or bottle can easily measure the amount of urine…the patient won’t thank you if you unnecessarily give them a catheter-induced infection…or a paraphymosis!
A complete myeloma screen comprises of…immunoglobulins, serum electrophoresis, urine bence jones AND serum free light chains….often the first two/three are normal and the last one reveals the diagnosis but is often never checked! And remember…a urine PCR will miss those myeloma casts in the urine so check a urine ACR instead!
If pyrexial with a dialysis line – culture the line…and if very sick with suspected line sepsis…let us/ITU know and remove the line before the patient rapidly deteriorates…
Be confident with your fluid status assessment and stick to a plan – there’s no such thing as IV fluid with furosemide to keep it off the chest! Either give fluid or diurese…
Is the patient passing urine?? If anuric, the patient is unlikely to be biochemically safe in 12-24 hours so speak to us early before the potassium or pulmonary oedema is too severe to transfer the patient
Before labelling a patient as ‘anuric’ with AKI…check the catheter isn’t clamped first – it’s not ideal to have to dialyse an iatrogenic obstruction
Obstruction…obstructed patients can still pass urine. Obstructed patients don’t always have hydronephrosis (scarred kidneys don’t stretch as well). Obstructed patients can have a normal bladder scan. Obstructive patients can have painless obstruction. Obstructed patients need urology to un-obstruct them…
Causes of AKI not to miss…obstruction (do a renal tract US), rhabdomyolysis (check a CK), vasculitis (check ANCAs), genetic form of aHUS (if TMA – quickly refer to renal), oxalate nephropathy (scope the urine and check oxalate)
Fever/prodromal symptoms and renal impairment – is this vasculitis??? Fever not responding to Abx…is this vasculitis??? AND check a ferritin – is this HLH? >4k = suspicion, >10k is poor sign…
If you’re going to catheterise that AKI ?retention – make sure you do and DOCUMENT the post-micturition bladder scan BEFORE the catheter AND the post-catheter volume of urine drained….otherwise we will be wondering if there was ever genuine retention 2 weeks later when the sCr is still stuck at 800…
Insulin-dextrose is not a risk-free treatment…carefully monitor glucose to avoid a potential hypoglycaemic death….And don’t forget – it is a K+ hiding therapy to buy you time to fix the underlying cause of hyperkalaemia…
Take loin pain seriously in the context of renal impairment and it isn’t always due to stones and clot retention…also consider renal infarction/vessel thrombosis and intrinsic renal pathologies (AIN, IgAN, crystalopathies)
Don’t call us to ask what antibiotic to prescribe in CKD…you decide what you want to give the patient and we can advise on dose alteration…but if you can get hold of a RENAL PHARMACIST they are GOLD!
The components of a renal screen are…blood film, stool culture and STEC, ESR, CK, CMV, EBV, ASOT, hep/HIV serology, MSU, autoAb screen, serum free light chains, immunoglobulins, electrophoresis (serum/urine), uACR, uPCR, complement, RhF, ENA, ANCA, anti-GBM, ant-centromere Ab, Anti-SCL-70 and cryoglobulins BUT what you send depends on each patient so we will advise…
Don’t sit on renal impairment without a clear cause without involving us…you may be missing something life-threatening (such as vasculitis) or something reversible (like myeloma cast nephropathy or obstruction) and there may be time left to rectify this before permanent damage occurs..
There’s absolutely no point in giving diuretics without carefully educating the patient about a salt and fluid restriction…they’ll be annoyed when they realise you haven’t told them
If you need to do a CT for something that will influence your management of a serious/life-threatening problem (i.e. acute abdomen) then please do the scan…don’t worry about the renal function!
There are only a few ‘true/genuine’ nephrotoxins…e.g. aminoglycoside antibiotics, amphotericin B, cisplatin…other drugs have a ‘haemodynamic effect on GFR’ and are NOT nephrotoxic…e.g. ACEi/ARBs and NSAIDs…some drugs have been shown to cause interstitial nephritis in SOME patients/rare cases…e.g. beta-lactam antibiotics, NSAIDS, PPIs….and some drugs that can cause renal impairment in other ways in rare scenarios…e.g. Penicillamine, GOLD, Lithium etc.
If you have a fluid overloaded patient with renal impairment…do not stop diuretics (or their ACEi) because the sCr is getting worse! If they have too much fluid on board – you will only risk worsening pulmonary oedema when you stop their diuretics! The commonest reason for readmission after AKI is with pulmonary oedema…don’t stop diuretics without a review and re-initiation plan…
If you see a patient with problematic chronic leg oedema and/or ‘chronic leg cellulitis’ on pregabalin…STOP the pregabalin! They’ll thank you for avoiding long hospital admissions, reduced mobility and countless diuretic dose increases when it goes away…pregabalin induced lower limb oedema is MUCH more common than you think!
If a patient’s serum albumin is low and they have any degree of oedema – do a urine PCR! You’ll save them an admission for ‘heart failure’ when you diagnose their nephrotic syndrome…
Renal phenotypes…know this…CKD/dialysis patients get sepsis and cardiovascular disease….weird stuff happens in transplant patients (unusual infections/cancers/metabolic things)…and always take skin lesions/rashes, loin pain and headaches seriously in renal patients
ACEi dilate the efferent arteriole and NSAIDs constrict the afferent arteriole causing glomerular ischaemia in combination and can result in end stage kidney failure…believe it or not, we see this all the time and damage is not always reversible…
ACEi/ARBs slow progression of proteinuric CKD and improve mortality in HFrEF…do not tell your patient that they are ‘poisonous’ to their kidneys. Don’t prescribe if hyperkalaemic or in severe bilateral renal artery stenosis AND only suspend if acute illness (sepsis, hypovolaemia, hypotension) or hyperkalaemia. When you STOP them, you MUST communicate and document a review date and indication for restarting the drug. You wouldn’t stop a patient’s chemotherapy without a plan so don’t do this here too…AND WRITE THE REVIEW PLANS CLEARLY IN THE DISCHARGE SUMMARY
Chronic hypertension is a longstanding issue that does not warrant escalation of treatment as an inpatient (unless acute symptoms). The half-life of Amlodipine is 35-50 hours and Doxazocin is 22 hours so don’t ramp up their BP medications in hospital as takes weeks to make an impact on BP…you’ll also encourage non-compliance with all the side-effects of the extra medications and the patient will be in a mess
We want to see patients URGENTLY as an outpatient if new diagnosis of nephrotic syndrome or stage 1 or 2 AKI not sue to sepsis/hypovolaemia/hypotension
Renal transplant tips….monitor their trough tacrolimus/ciclosporin levels, DO NOT suspend their immunosuppression without consulting the renal team (would want MMF/Azathioprine suspended usually in sepsis) and hydrocortisone half-life is about 1.5 hours so ensure a TDS/QDS regime when converted from Prednisolone and an accurate dose conversion (1mg prednisolone = 4mg hydrocortisone)
Some drugs that increase tacrolimus levels…clarithromycin/erythromycin, fluconazole, clotrimazole diltiazem, nifedipine, grapefruit juice (tac toxicity = tremor, AKI) and some drugs that decrease tacrolimus levels…carbamazepine, phenytoin, rifabutin, rifampicin, antacids, St John’s wort (subtherapeutic tac = transplant rejection and graft loss) so CHECK interactions for ALL new meds
eGFR is most often measured in lab with either MDRD or CKD-EEPI formulae. Creatinine-clearance (Cockroft/Gault formula) relies on age/gender/weight to estimate GFR (not body size) so it’s more accurate if muscle mass is extremely high but unreliable in obesity…although the BNF relies on this formula for drug dosing – it’s not that much more accurate. True GFR should be measured using 24h creatinine clearance (using 24 hr urine) or by isotope GFR measurement.
URINE GOOD HANDS 